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        <title>Angiogenesis via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Angiogenesis' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Angiogenesis&t=Angiogenesis&s=Search&f=source]]></link>
        <lastBuildDate>Mon, 06 Feb 2012 16:52:00 +0100</lastBuildDate>
        <item>
            <title>Binding and neutralization of vascular endothelial growth factor (VEGF) and related ligands by VEGF Trap, ranibizumab and bevacizumab</title>
            <link>http://www.medworm.com/index.php?rid=5664290&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fdq1451519r56l403%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Pharmacological inhibition of VEGF-A has proven to be effective in inhibiting angiogenesis and vascular leak associated with
 cancers and various eye diseases. However, little information is currently available on the binding kinetics and relative
 biological activity of various VEGF inhibitors. Therefore, we have evaluated the binding kinetics of two anti-VEGF antibodies,
 ranibizumab and bevacizumab, and VEGF Trap (also known as aflibercept), a novel type of soluble decoy receptor, with substantially
 higher affinity than conventional soluble VEGF receptors. VEGF Trap bound to all isoforms of human VEGF-A tested with subpicomolar
 affinity. Ranibizumab and bevacizumab also bound human VEGF-A, but with markedly lower affinity. The association rate for
 VEGF Trap bindin...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5664290</comments>
            <pubDate>Thu, 02 Feb 2012 18:09:18 +0100</pubDate>
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        <item>
            <title>CD34 marks angiogenic tip cells in human vascular endothelial cell cultures</title>
            <link>http://www.medworm.com/index.php?rid=5617048&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr022156022976826%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The functional shift of quiescent endothelial cells into tip cells that migrate and stalk cells that proliferate is a key
 event during sprouting angiogenesis. We previously showed that the sialomucin CD34 is expressed in a small subset of cultured
 endothelial cells and that these cells extend filopodia: a hallmark of tip cells in vivo. In the present study, we characterized
 endothelial cells expressing CD34 in endothelial monolayers in vitro. We found that CD34-positive human umbilical vein endothelial
 cells show low proliferation activity and increased mRNA expression of all known tip cell markers, as compared to CD34-negative
 cells. Genome-wide mRNA profiling analysis of CD34-positive endothelial cells demonstrated enrichment for biological functions
 related to ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5617048</comments>
            <pubDate>Tue, 17 Jan 2012 07:18:44 +0100</pubDate>
            <guid isPermaLink="false">5617048</guid>        </item>
        <item>
            <title>A phase II study of neoadjuvant bevacizumab plus capecitabine and concomitant radiotherapy in patients with locally advanced rectal cancer</title>
            <link>http://www.medworm.com/index.php?rid=5568910&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F6820n43h52080430%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;The schedule of neoadjuvant therapy tested was safe and active. Pre-treatment vessel density by the panendothelial marker
 anti CD-34 antibody, post-treatment Ki-67 labeling index and VEGFR-2 expression were significantly associated to residual
 tumor area. The biomarkers correlations warrant further evaluation in prospective clinical trials.
 
 
 
 
	Content Type Journal ArticleCategory Original PaperPages 1-10DOI 10.1007/s10456-011-9250-0Authors
		Giampietro Gasparini, Unità Operativa Complessa di Oncologia Medica, Azienda Complesso Ospedaliero di Rilevanza Nazionale “S. Filippo Neri”, Via G. Martinotti, 20, 00135 Rome, ItalyFrancesco Torino, Unità Operativa Complessa di Oncologia Medica, Azienda Complesso Ospedaliero di Rilevanza Nazionale “S. Filippo Neri...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568910</comments>
            <pubDate>Mon, 02 Jan 2012 16:46:32 +0100</pubDate>
            <guid isPermaLink="false">5568910</guid>        </item>
        <item>
            <title>Down-modulation of TNFSF15 in ovarian cancer by VEGF and MCP-1 is a pre-requisite for tumor neovascularization</title>
            <link>http://www.medworm.com/index.php?rid=5568911&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx2u55j722087632u%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Persistent inflammation and neovascularization are critical to cancer development. In addition to upregulation of positive
 control mechanisms such as overexpression of angiogenic and inflammatory factors in the cancer microenvironment, loss of otherwise
 normally functioning negative control mechanisms is likely to be an important attribute. Insights into the down-modulation
 of such negative control mechanisms remain largely unclear, however. We show here that tumor necrosis factor superfamily-15
 (TNFSF15), an endogenous inhibitor of neovascularization, is a critical component of the negative control mechanism that operates
 in normal ovary but is missing in ovarian cancer. We show in clinical settings that TNFSF15 is present prominently in the
 vasculature of normal...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568911</comments>
            <pubDate>Fri, 30 Dec 2011 16:50:14 +0100</pubDate>
            <guid isPermaLink="false">5568911</guid>        </item>
        <item>
            <title>Exosomes released by K562 chronic myeloid leukemia cells promote angiogenesis in a src-dependent fashion</title>
            <link>http://www.medworm.com/index.php?rid=5556789&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx6134j4p07500m32%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Exosomes, microvesicles of endocytic origin released by normal and tumor cells, play an important role in cell-to-cell communication.
 Angiogenesis has been shown to regulate progression of chronic myeloid leukemia (CML). The mechanism through which this happens
 has not been elucidated. We isolated and characterized exosomes from K562 CML cells and evaluated their effects on human umbilical
 endothelial cells (HUVECs). Fluorescent-labeled exosomes were internalized by HUVECs during tubular differentiation on Matrigel.
 Exosome localization was perinuclear early in differentiation, moving peripherally in cells undergoing elongation and connection.
 Exosomes move within and between nanotubular structures connecting the remodeling endothelial cells. They stimulated angiot...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5556789</comments>
            <pubDate>Tue, 27 Dec 2011 17:01:16 +0100</pubDate>
            <guid isPermaLink="false">5556789</guid>        </item>
        <item>
            <title>CLT1 targets angiogenic endothelium through CLIC1 and fibronectin</title>
            <link>http://www.medworm.com/index.php?rid=5556790&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F6w6k12782252l156%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Angiogenesis is important for tumor growth and metastasis. CLT1 (CGLIIQKNEC), a peptide that binds to tumor interstitial spaces
 in the presence of fibrin-fibronectin, has structural similarity to the anti-angiogenic β-sheet peptides anastellin and anginex.
 This similarity is reflected in the ability of CLT1 to form co-aggregates with fibronectin that induce an unfolded protein
 response and cause autophagic cell death in proliferating endothelial cells. CLT1 cytotoxicity is mediated at least in parts
 by a novel CLT1 binding protein, Chloride Intracellular Channel 1 (CLIC1), which promotes internalization of CLT1-fibronectin
 co-aggregates in a mechanism that depends on the LIIQK amino acid sequence of CLT1. LIIQK encompasses amino acid residues
 relevant for CLT1 bi...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5556790</comments>
            <pubDate>Tue, 27 Dec 2011 17:01:14 +0100</pubDate>
            <guid isPermaLink="false">5556790</guid>        </item>
        <item>
            <title>MG624, an α7-nAChR antagonist, inhibits angiogenesis via the Egr-1/FGF2 pathway</title>
            <link>http://www.medworm.com/index.php?rid=5549804&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fn52061352244545w%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Small cell lung cancer (SCLC) demonstrates a strong etiological association with smoking. Although cigarette smoke is a mixture
 of about 4,000 compounds, nicotine is the addictive component of cigarette smoke. Several convergent studies have shown that
 nicotine promotes angiogenesis in lung cancers via the α7-nicotinic acetylcholine receptor (α7-nAChR) on endothelial cells.
 Therefore, we conjectured that α7-nAChR antagonists may attenuate nicotine-induced angiogenesis and be useful for the treatment
 of human SCLC. For the first time, our study explores the anti-angiogenic activity of MG624, a small-molecule α7-nAChR antagonist,
 in several experimental models of angiogenesis. We observed that MG624 potently suppressed the proliferation of primary human
 microvas...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549804</comments>
            <pubDate>Sat, 24 Dec 2011 16:45:49 +0100</pubDate>
            <guid isPermaLink="false">5549804</guid>        </item>
        <item>
            <title>Inhibition of hemangioma development in a syngeneic mouse model correlates with bcl-2 suppression and the inhibition of Akt kinase activity</title>
            <link>http://www.medworm.com/index.php?rid=5549805&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F65002252t6111418%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;Our observations reveal possible mechanisms for the inhibitory effects of bleomycin on hemangiomagenesis, and raise the possibility
 that bcl-2 might be an important therapeutic target in the treatment of hemangiomas.
 
 
 
 
	Content Type Journal ArticleCategory Original PaperPages 1-9DOI 10.1007/s10456-011-9248-7Authors
		Peace Mabeta, Department of Physiology, Faculty of Health Sciences, University of Pretoria, P.O. Box 2034, Pretoria, 0001 South AfricaMichael S. Pepper, Department of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria, South Africa
	

	
		Journal AngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5549805</comments>
            <pubDate>Sat, 24 Dec 2011 16:45:48 +0100</pubDate>
            <guid isPermaLink="false">5549805</guid>        </item>
        <item>
            <title>In vivo laser speckle imaging reveals microvascular remodeling and hemodynamic changes during wound healing angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=5542220&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fn4n12426103857m8%2F</link>
            <description>In this study, we demonstrate the utility of LSCI for characterizing
 microvascular remodeling and hemodynamic changes during wound healing angiogenesis in vivo. A 2&amp;nbsp;mm diameter hole was made
 in the mouse ear and the periphery of the wound imaged in vivo using LSCI over 12&amp;nbsp;days. We were able to visualize and quantify
 the vascular and perfusion changes that accompanied wound healing in the microenvironment proximal to the wound, and validated
 these changes with histology. We found that consistent with the stages of wound healing, microvessel density increased during
 the initial inflammatory phase (i.e., day 0–3), stayed elevated through the tissue formation phase (i.e., until day 7) and
 returned to baseline during the tissue remodeling phase (i.e., by day 12). Concomitant ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5542220</comments>
            <pubDate>Fri, 23 Dec 2011 16:54:18 +0100</pubDate>
            <guid isPermaLink="false">5542220</guid>        </item>
        <item>
            <title>Foretinib demonstrates anti-tumor activity and improves overall survival in preclinical models of hepatocellular carcinoma</title>
            <link>http://www.medworm.com/index.php?rid=5542221&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx75374nx11414886%2F</link>
            <description>This study provides a compelling
 rationale for clinical investigation in patients with advanced HCC.
 
 
 
 
	Content Type Journal ArticleCategory Original PaperPages 1-12DOI 10.1007/s10456-011-9243-zAuthors
		Hung Huynh, Laboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, 11 Hospital Drive, Singapore, 169610 SingaporeRichard Ong, Laboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, 11 Hospital Drive, Singapore, 169610 SingaporeKhee Chee Soo, Laboratory of Molecular Endocrinology, Division of Molecular and Cellular Research, National Cancer Centre, 11 Hospital Drive, Singapore, 169610 Singapore
	

	
		Journal AngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogen...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5542221</comments>
            <pubDate>Tue, 20 Dec 2011 16:45:06 +0100</pubDate>
            <guid isPermaLink="false">5542221</guid>        </item>
        <item>
            <title>Silencing TRPM7 mimics the effects of magnesium deficiency in human microvascular endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=5533470&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk137081217458v22%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Evidence has accumulated to suggest that magnesium might play a role in controlling angiogenesis. Since microvascular endothelial
 cells are protagonists in this process, we investigated the behavior of these cells cultured in low extracellular magnesium
 or silenced for its transporter Transient Receptor Potential Melastatin (TRPM)7, essential for cellular magnesium homeostasis.
 In particular, we focused on some crucial steps of the angiogenic process, i.e. proliferation, migration, protease production
 and organization in tridimensional structures. Silencing TRPM7 mimics the effects of low extracellular magnesium on human
 microvascular endothelial cells (HMEC). Indeed, while no effects were observed on the production of metalloproteases and on
 tridimensional organi...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5533470</comments>
            <pubDate>Mon, 19 Dec 2011 16:53:33 +0100</pubDate>
            <guid isPermaLink="false">5533470</guid>        </item>
        <item>
            <title>Therapeutic angiogenesis for myocardial ischemia revisited: basic biological concepts and focus on latest clinical trials</title>
            <link>http://www.medworm.com/index.php?rid=5465217&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F35042201m466234r%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Therapeutic angiogenesis is based on the premise that the development of new blood vessels can be augmented by exogenous administration
 of the appropriate growth factors. Over the last years, successful preclinical studies and promising results of early clinical
 trials have created great excitement about the potential of therapeutic angiogenesis for patients with advanced ischemic heart
 disease. The authors provide an overview of the biology of angiogenesis, the basic characteristics of angiogenic factors,
 and the different routes of their delivery. They discuss experimental studies in animal models of myocardial ischemia and
 outline available clinical studies on therapeutic angiogenesis for myocardial ischemia. Related safety issues are also addressed
 followed by...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5465217</comments>
            <pubDate>Sat, 26 Nov 2011 16:48:04 +0100</pubDate>
            <guid isPermaLink="false">5465217</guid>        </item>
        <item>
            <title>The targeted delivery of IL17 to the mouse tumor neo-vasculature enhances angiogenesis but does not reduce tumor growth rate</title>
            <link>http://www.medworm.com/index.php?rid=5396835&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp74655801g250054%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;There has been a long controversy as to whether interleukin-17 (IL17) has an impact on tumor growth. In order to assess whether
 IL17 may affect tumor growth, it would be convenient to achieve high levels of this pro-inflammatory cytokine at the tumor
 neo-vasculature, since IL17 is known to promote angiogenesis. Here, we have generated and tested in vivo a fusion protein,
 consisting of the F8 antibody (specific to the alternatively spliced EDA domain of fibronectin, a marker of angiogenesis)
 and of murine IL17 (mIL17). The resulting immunocytokine (termed F8-mIL17) was shown to selectively localize at the tumor
 neo-vasculature and to vigorously promote tumor angiogenesis, without however reducing or enhancing tumor growth rate both
 in immunocompetent and in immunod...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5396835</comments>
            <pubDate>Thu, 03 Nov 2011 16:56:26 +0100</pubDate>
            <guid isPermaLink="false">5396835</guid>        </item>
        <item>
            <title>Reduced pathological angiogenesis and tumor growth in mice lacking GPR4, a proton sensing receptor</title>
            <link>http://www.medworm.com/index.php?rid=5375466&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm425638237731533%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The G protein-coupled receptor GPR4 is activated by acidic pH and recent evidence indicates that it is expressed in endothelial
 cells. In agreement with these reports, we observe a high correlation of GPR4 mRNA expression with endothelial marker genes,
 and we confirm expression and acidic pH dependent function of GPR4 in primary human vascular endothelial cells. GPR4-deficient
 mice were generated; these are viable and fertile and show no gross abnormalities. However, these animals show a significantly
 reduced angiogenic response to VEGF (vascular endothelial growth factor), but not to bFGF (basic fibroblast growth factor),
 in a growth factor implant model. Accordingly, in two different orthotopic models, tumor growth is strongly reduced in mice
 lacking GPR4. Histo...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5375466</comments>
            <pubDate>Tue, 01 Nov 2011 16:52:51 +0100</pubDate>
            <guid isPermaLink="false">5375466</guid>        </item>
        <item>
            <title>Prednisolone treatment reduces endometrial spiral artery development in women with recurrent miscarriage</title>
            <link>http://www.medworm.com/index.php?rid=5310786&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F4240213j201r70q1%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;The effect of prednisolone therapy for some women with RM may be due to altered endometrial angiogenic growth factor expression
 and reduced blood vessel maturation.
 
 
 
 
	Content Type Journal ArticleCategory Original PaperPages 1-10DOI 10.1007/s10456-011-9237-xAuthors
		Gendie E. Lash, Reproductive and Vascular Biology Group, Institute of Cellular Medicine, Newcastle University, 3rd Floor, William Leech Building, Newcastle upon Tyne, NE2 4HH UKJudith N. Bulmer, Reproductive and Vascular Biology Group, Institute of Cellular Medicine, Newcastle University, 3rd Floor, William Leech Building, Newcastle upon Tyne, NE2 4HH UKBarbara A. Innes, Reproductive and Vascular Biology Group, Institute of Cellular Medicine, Newcastle University, 3rd Floor, William Leech Building...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5310786</comments>
            <pubDate>Sat, 08 Oct 2011 15:42:15 +0100</pubDate>
            <guid isPermaLink="false">5310786</guid>        </item>
        <item>
            <title>Spatial dependence of alveolar angiogenesis in post-pneumonectomy lung growth</title>
            <link>http://www.medworm.com/index.php?rid=5301843&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr762472600g21107%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Growth of the remaining lung after pneumonectomy has been observed in many mammalian species; nonetheless, the pattern and
 morphology of alveolar angiogenesis during compensatory growth is unknown. Here, we investigated alveolar angiogenesis in
 a murine model of post-pneumonectomy lung growth. As expected, the volume and weight of the remaining lung returned to near-baseline
 levels within 21&amp;nbsp;days of pneumonectomy. The percentage increase in lobar weight was greatest in the cardiac lobe (P&amp;nbsp;&amp;lt;&amp;nbsp;0.001). Cell cycle flow cytometry demonstrated a peak of lung cell proliferation (12.02&amp;nbsp;±&amp;nbsp;1.48%) 6&amp;nbsp;days after pneumonectomy.
 Spatial autocorrelation analysis of the cardiac lobe demonstrated clustering of similar vascular densities (positive auto...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5301843</comments>
            <pubDate>Tue, 04 Oct 2011 05:52:09 +0100</pubDate>
            <guid isPermaLink="false">5301843</guid>        </item>
        <item>
            <title>Ginsenoside-Rg1 mediates a hypoxia-independent upregulation of hypoxia-inducible factor-1α to promote angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=5292959&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fbr61v73784831252%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Hypoxia-inducible factor (HIF-1) is the key transcription regulator for multiple angiogenic factors and is an appealing target.
 Ginsenoside-Rg1, a nontoxic saponin isolated from the rhizome of Panax ginseng, exhibits potent proangiogenic activity and has the potential to be developed as a new angiotherapeutic agent. However, the
 mechanisms by which Rg1 promotes angiogenesis are not fully understood. Here, we show that Rg1 is an effective stimulator
 of HIF-1α under normal cellular oxygen conditions in human umbilical vein endothelial cells. HIF-1α steady-state mRNA was
 not affected by Rg1. Rather, HIF-1α protein synthesis was stimulated by Rg1. This effect was associated with constitutive
 activation of phosphatidylinositol 3-kinase (PI3K)/Akt and its effector p70...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5292959</comments>
            <pubDate>Sun, 02 Oct 2011 05:47:51 +0100</pubDate>
            <guid isPermaLink="false">5292959</guid>        </item>
        <item>
            <title>Chronic hypoxia impairs extracellular nucleotide metabolism and barrier function in pulmonary artery vasa vasorum endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=5233512&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F050325n312040070%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Vascular remodeling plays a pivotal role in a variety of pathophysiological conditions where hypoxia and inflammation are
 prominent features. Intravascular ATP, ADP and adenosine are known as important regulators of vascular tone, permeability
 and homeostasis, however contribution of purinergic signalling to endothelial cell growth and angiogenesis remains poorly
 understood. By using vasa vasorum endothelial cells (VVEC) isolated from pulmonary artery adventitia of control and chronically
 hypoxic neonatal calves, these studies were aimed to evaluate the effect of hypoxia on biochemical and functional properties
 of microvascular endothelial network at the sites of angiogenesis. In comparison with normoxic controls, VVEC from hypoxic
 animals are characterized by (1)...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5233512</comments>
            <pubDate>Fri, 16 Sep 2011 05:44:55 +0100</pubDate>
            <guid isPermaLink="false">5233512</guid>        </item>
        <item>
            <title>Monitoring antivascular therapy in head and neck cancer xenografts using contrast-enhanced MR and US imaging</title>
            <link>http://www.medworm.com/index.php?rid=5217700&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl712884q48793474%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;These findings demonstrate that both CE-MRI and CE-US allow monitoring of early changes in vascular function following VDA
 therapy. The results also demonstrate, for the first time, potent vascular disruptive and antitumor activity of DMXAA against
 patient tumor-derived head and neck carcinoma xenografts.
 
 
 
 
	Content Type Journal ArticleCategory Original PaperPages 1-11DOI 10.1007/s10456-011-9233-1Authors
		Mukund Seshadri, Department of Pharmacology and Therapeutics, Preclinical Imaging Laboratory, Roswell Park Cancer Institute, Buffalo, NY, USANuno T. Sacadura, VisualSonics Inc., Toronto, ON, CanadaTonya Coulthard, VisualSonics Inc., Toronto, ON, Canada
	

	
		Journal AngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5217700</comments>
            <pubDate>Thu, 08 Sep 2011 05:57:58 +0100</pubDate>
            <guid isPermaLink="false">5217700</guid>        </item>
        <item>
            <title>Bevacizumab in the treatment of high-grade gliomas: an overview</title>
            <link>http://www.medworm.com/index.php?rid=5155693&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fgj01736433737378%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Angiogenesis is a process that is integral to the pathogenesis of high-grade gliomas. Bevacizumab, a humanized monoclonal
 antibody against vascular endothelial growth factor has emerged as an important therapeutic agent. Data from clinical trials
 in both recurrent and newly-diagnosed gliomas have shown improved radiological responses and quality of life with acceptable
 morbidity. However, an improvement in overall survival has not yet been seen and there are concerns on possible change in
 the pattern of relapse following therapy. Several unanswered questions remain including the dose, timing and sequencing that
 warrant further research.
 
 
	Content Type Journal ArticleCategory Review PaperPages 1-8DOI 10.1007/s10456-011-9232-2Authors
		Saroj Kunnakkat, Department ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5155693</comments>
            <pubDate>Sat, 20 Aug 2011 15:50:57 +0100</pubDate>
            <guid isPermaLink="false">5155693</guid>        </item>
        <item>
            <title>Tumor kinase activity in locally advanced rectal cancer: angiogenic signaling and early systemic dissemination</title>
            <link>http://www.medworm.com/index.php?rid=5129947&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx3642085365r6568%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Tumor hypoxia is a common determinant of resistance to cytotoxic therapies and metastatic behavior. In rectal cancer patients
 receiving preoperative chemoradiotherapy, tyrosine kinase activities in tumors with poor and good treatment responses were
 found to differ. Given that tyrosine kinase signaling mediates hypoxic tissue adaptation, the present study examined whether
 tumor kinase activity might also correlate with systemic dissemination of rectal cancer. Immunomagnetic selection of disseminated
 tumor cells (DTC) from bone marrow aspirates was undertaken in 55 patients with locally advanced rectal cancer. Using peptide
 arrays with 144 tyrosine kinase substrates, phosphopeptide signatures were generated from patients’ baseline tumor biopsies,
 to study associat...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5129947</comments>
            <pubDate>Thu, 11 Aug 2011 06:56:11 +0100</pubDate>
            <guid isPermaLink="false">5129947</guid>        </item>
        <item>
            <title>Heme oxygenase 1 (HO-1) challenges the angiogenic switch in prostate cancer</title>
            <link>http://www.medworm.com/index.php?rid=5129946&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F700r508826324433%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Prostate cancer (PCa) is the second leading cause of cancer-associated death in men. Once a tumor is established it may attain
 further characteristics via mutations or hypoxia, which stimulate new blood vessels. Angiogenesis is a hallmark in the pathogenesis
 of cancer and inflammatory diseases that may predispose to cancer. Heme oxygenase-1 (HO-1) counteracts oxidative and inflammatory
 damage and was previously reported to play a key role in prostate carcinogenesis. To gain insight into the anti-tumoral properties
 of HO-1, we investigated its capability to modulate PCa associated-angiogenesis. In the present study, we identified in PC3
 cells a set of inflammatory and pro-angiogenic genes down-regulated in response to HO-1 overexpression, in particular VEGFA,
 VEGFC...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5129946</comments>
            <pubDate>Thu, 11 Aug 2011 06:56:11 +0100</pubDate>
            <guid isPermaLink="false">5129946</guid>        </item>
        <item>
            <title>Pro-angiogenic hematopoietic progenitor cells and endothelial colony-forming cells in pathological angiogenesis of bronchial and pulmonary circulation</title>
            <link>http://www.medworm.com/index.php?rid=5076404&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb887716mj14m1114%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Dysregulation of angiogenesis is a common feature of many disease processes. Vascular remodeling is believed to depend on
 the participation of endothelial progenitor cells, but the identification of endothelial progenitors in postnatal neovascularization
 remains elusive. Current understanding posits a role for circulating pro-angiogenic hematopoietic cells that interact with
 local endothelial cells to establish an environment that favors angiogenesis in physiologic and pathophysiologic responses.
 In the lung, increased and dysregulated angiogenesis is a hallmark of diseases of the bronchial and pulmonary circulations,
 manifested by asthma and pulmonary arterial hypertension (PAH), respectively. In asthma, THelper-2 immune cells produce angiogenic factors that mobil...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5076404</comments>
            <pubDate>Wed, 27 Jul 2011 15:48:35 +0100</pubDate>
            <guid isPermaLink="false">5076404</guid>        </item>
        <item>
            <title>Examining the role of Rac1 in tumor angiogenesis and growth: a clinically relevant RNAi-mediated approach</title>
            <link>http://www.medworm.com/index.php?rid=5076405&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fhj472324341q3w17%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Angiogenesis, the sprouting of new blood vessels from the pre-existing vasculature, is a well established target in anti-cancer
 therapy. It is thought that the Rho GTPase Rac1 is required during vascular endothelial growth factor (VEGF)-mediated angiogenesis.
 In the present study, we have used a clinically relevant RNA interference approach to silence Rac1 expression. Human umbilical
 vein endothelial cells were transiently transfected with non-specific control siRNA (siNS) or Rac1 siRNA (siRac1) using electroporation
 or Lipofectamine 2000. Functional assays with transfected endothelial cells were performed to determine the effect of Rac1
 knockdown on angiogenesis in vitro. Silencing of Rac1 inhibited VEGF-mediated tube formation, cell migration, invasion and
 proli...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5076405</comments>
            <pubDate>Tue, 26 Jul 2011 05:48:37 +0100</pubDate>
            <guid isPermaLink="false">5076405</guid>        </item>
        <item>
            <title>Anti-CXCL5 therapy ameliorates IL-17-induced arthritis by decreasing joint vascularization</title>
            <link>http://www.medworm.com/index.php?rid=5061506&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fq3k2057340042226%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;IL-17-induced joint inflammation is associated with increased angiogenesis. However, the mechanism by which IL-17 mediates
 angiogenesis is undefined. Therefore, the pathologic role of CXCL1 and CXCL5 was investigated in arthritis mediated by local
 expression of IL-17, employing a neutralizing antibody to each chemokine. Next, endothelial chemotaxis was utilized to examine
 whether endothelial migration was differentially mediated by CXCL1 and CXCL5. Our results demonstrate that IL-17-mediated
 disease activity was not affected by anti-CXCL1 treatment alone. In contrast, mice receiving anti-CXCL5 demonstrated significantly
 reduced clinical signs of arthritis, compared to the mice treated with IgG control. Consistently, while inflammation, synovial
 lining thickness, b...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5061506</comments>
            <pubDate>Thu, 21 Jul 2011 18:06:41 +0100</pubDate>
            <guid isPermaLink="false">5061506</guid>        </item>
        <item>
            <title>Retraction Note: Gold nanoparticles inhibit vascular endothelial growth factor-induced angiogenesis and vascular permeability via Src dependent pathway in retinal endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=5061507&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F90x6hu16618222u1%2F</link>
            <description>Content Type Journal ArticlePages 1-2DOI 10.1007/s10456-011-9225-1Authors
		Kalimuthu Kalishwaralal, Department of Biotechnology, Division of Molecular and Cellular Biology, Kalasalingam University (Kalasalingam Academy of Research and Education), Anand Nagar, Krishnankoil, Tamilnadu 626 190, IndiaSardarpasha Sheikpranbabu, Department of Biotechnology, Division of Molecular and Cellular Biology, Kalasalingam University (Kalasalingam Academy of Research and Education), Anand Nagar, Krishnankoil, Tamilnadu 626 190, IndiaSelvaraj BarathManiKanth, Department of Biotechnology, Division of Molecular and Cellular Biology, Kalasalingam University (Kalasalingam Academy of Research and Education), Anand Nagar, Krishnankoil, Tamilnadu 626 190, IndiaRavinarayanan Haribalaganesh, Department of Biotec...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5061507</comments>
            <pubDate>Tue, 19 Jul 2011 23:38:59 +0100</pubDate>
            <guid isPermaLink="false">5061507</guid>        </item>
        <item>
            <title>Retraction Note: PEDF inhibits VEGF- and EPO- induced angiogenesis in retinal endothelial cells through interruption of PI3K/Akt phosphorylation</title>
            <link>http://www.medworm.com/index.php?rid=5057259&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F17217t45p815w111%2F</link>
            <description>Content Type Journal ArticlePages 1-2DOI 10.1007/s10456-011-9224-2Authors
		Banumathi Elayappan, Department of Biotechnology, Division of Molecular and Cellular Biology, Kalasalingam University (Kalasalingam Academy of Research and Education), Anand Nagar, Krishnankoil, Madurai, Tamil Nadu 626190, IndiaHaribalaganesh Ravinarayannan, Department of Biotechnology, Division of Molecular and Cellular Biology, Kalasalingam University (Kalasalingam Academy of Research and Education), Anand Nagar, Krishnankoil, Madurai, Tamil Nadu 626190, IndiaSheik Pran Babu Sardar Pasha, Department of Biotechnology, Division of Molecular and Cellular Biology, Kalasalingam University (Kalasalingam Academy of Research and Education), Anand Nagar, Krishnankoil, Madurai, Tamil Nadu 626190, IndiaKyung-jin Lee, Depa...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5057259</comments>
            <pubDate>Mon, 18 Jul 2011 15:53:27 +0100</pubDate>
            <guid isPermaLink="false">5057259</guid>        </item>
        <item>
            <title>Suppression of neovascularization and experimental arthritis by D-form of anti-flt-1 peptide conjugated with mini-PEG™</title>
            <link>http://www.medworm.com/index.php?rid=5035421&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F483581834u514r8v%2F</link>
            <description>In conclusion, our data suggests that mini-PEGylated
 allD is more beneficial in the treatment of RA than unmodified anti-flt-1 peptides, since it has increased stability and the
 possibility of oral delivery, and could be applied to treat angiogenesis-dependent human diseases, including RA.
 
 
	Content Type Journal ArticlePages 1-12DOI 10.1007/s10456-011-9226-0Authors
		Jin-Sun Kong, Research Institute of Immunobiology, Catholic Research Institute of Medical Science, Seoul, KoreaSeung-Ah Yoo, Research Institute of Immunobiology, Catholic Research Institute of Medical Science, Seoul, KoreaJong-Hoon Kang, Postech-Catholic Biomedical Engineering Institute, Catholic University of Korea, Seoul, KoreaWooree Ko, Department of Chemical Engineering, Pohang University of Science and Technology, Po...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5035421</comments>
            <pubDate>Wed, 13 Jul 2011 06:17:04 +0100</pubDate>
            <guid isPermaLink="false">5035421</guid>        </item>
        <item>
            <title>Cellular level characterization of capillary regression in inflammatory angiogenesis using an in vivo corneal model</title>
            <link>http://www.medworm.com/index.php?rid=5026856&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Frp301667287x1686%2F</link>
            <description>In this study, we introduce a technique for repeated, microscopic observation of single regressing capillaries in vivo in
 inflamed murine corneas. Natural capillary regression was initiated by removal of inflammatory stimulus during an active pro-angiogenic
 phase, while the additional impact of anti-angiogenic treatment with triamcinolone or bevazicumab was investigated. Capillaries
 regressed naturally within 1&amp;nbsp;week and treatments did not further enhance the natural regression. Morphologically, early-phase
 regression was characterized by significant lumen narrowing and a significant reduction in CD11b+ myeloid cell infiltration
 of the extracellular matrix. By 1&amp;nbsp;week, vascular remodeling occurred concomitant with CD11b+CD68+KiM2R+ mature macrophage
 localization on capillary ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5026856</comments>
            <pubDate>Sun, 10 Jul 2011 05:50:54 +0100</pubDate>
            <guid isPermaLink="false">5026856</guid>        </item>
        <item>
            <title>Effects of obstetric factors and storage temperatures on the yield of endothelial colony forming cells from umbilical cord blood</title>
            <link>http://www.medworm.com/index.php?rid=4997157&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F842v6618gp7l182m%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;As umbilical cord blood (UCB) is a rich source of endothelial colony-forming cells (ECFC), our aim was twofold: (1) to examine
 potential obstetric selection criteria for achieving the highest ECFC yields from UCB units, and (2) to determine whether
 transient storage temperatures of fresh UCB and cryopreservation of UCB units affected ECFC yield and function. ECFC quality
 was assessed before and after cryopreservation by their clonogenic proliferative potential. Of the 20 factors examined, placental
 weight was the only statistically significant obstetric factor that predicted ECFC frequency in UCB. Studies on the effects
 of storage revealed that transient storage of fresh UCB at 4°C reduced ECFC yield compared with storage at 22°C, while cryopreservation
 of UCB M...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4997157</comments>
            <pubDate>Thu, 30 Jun 2011 17:49:19 +0100</pubDate>
            <guid isPermaLink="false">4997157</guid>        </item>
        <item>
            <title>VEGF-C differentially regulates VEGF-A expression in ocular and cancer cells; promotes angiogenesis via RhoA mediated pathway</title>
            <link>http://www.medworm.com/index.php?rid=4974679&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F28t6873342k01885%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Vascular angiogenesis is regulated by a number of cytokines of which vascular endothelial growth factor (VEGF)-A/and its receptor
 vascular endothelial growth factor receptor 2 (VEGFR2) play an indisputable role. Similarly lymphangiogenesis is regulated
 by VEGF-C and its receptor VEGFR3. Currently for treating vasculogenesis diseases such as proliferative retinopathies and
 cancer, a number of anti-VEGF-A therapies are approved for clinical use. Although clinical efficacies achieved are remarkable,
 they are found to be transitory in nature, followed by restoration of anti-VEGF therapy resistant angiogenesis. Recently the
 regulatory role of VEGF-C in initiating and potentiating neo-angiogenesis has been uncovered. Although the interactive nature
 of VEGF-A and C is kn...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4974679</comments>
            <pubDate>Thu, 23 Jun 2011 06:00:35 +0100</pubDate>
            <guid isPermaLink="false">4974679</guid>        </item>
        <item>
            <title>A cell penetrating peptide derived from azurin inhibits angiogenesis and tumor growth by inhibiting phosphorylation of VEGFR-2, FAK and Akt</title>
            <link>http://www.medworm.com/index.php?rid=4932314&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa13111604247j67k%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Amino acids 50–77 (p28) of azurin, a 128 aa cupredoxin isolated from Pseudomonas aeruginosa, is essentially responsible for azurin’s preferential penetration of cancer cells. We now report that p28 also preferentially
 penetrates human umbilical vein endothelial cells (HUVEC), co-localized with caveolin-1 and VEGFR-2, and inhibits VEGF- and
 bFGF-induced migration, capillary tube formation and neoangiogenesis in multiple xenograft models. The antiangiogenic effect
 of p28 in HUVEC is associated with a dose-related non-competitive inhibition of VEGFR-2 kinase activity. However, unlike other
 antiangiogenic agents that inhibit the VEGFR-2 kinase, p28 decreased the downstream phosphorylation of FAK and Akt that normally
 precedes cellular repositioning of the cytoskele...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4932314</comments>
            <pubDate>Sat, 11 Jun 2011 06:31:47 +0100</pubDate>
            <guid isPermaLink="false">4932314</guid>        </item>
        <item>
            <title>EAF2 loss enhances angiogenic effects of Von Hippel-Lindau heterozygosity on the murine liver and prostate</title>
            <link>http://www.medworm.com/index.php?rid=4901305&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fd072212290k51534%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Von Hippel-Lindau (VHL) disease results from the inactivation of the VHL gene and is characterized by highly vascular tumors.
 A consequence of VHL loss is the stabilization of hypoxia-inducible factor (HIF) alpha subunits and increased expression of
 HIF target genes, which include pro-angiogenic growth factors such as vascular endothelial growth factor (VEGF). In mice,
 homozygous deletion of VHL is embryonic lethal due to vascular abnormalities in the placenta; and, VHL+/− mice develop proliferative vascular lesions in several major organs, most prominently the liver. Loss of ELL-associated factor
 (EAF2) in murine models has also been shown to induce increased vascular density in the liver as well as the prostate. Previously,
 EAF2 was determined to be a binding p...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4901305</comments>
            <pubDate>Fri, 03 Jun 2011 05:55:25 +0100</pubDate>
            <guid isPermaLink="false">4901305</guid>        </item>
        <item>
            <title>TM4SF1: a tetraspanin-like protein necessary for nanopodia formation and endothelial cell migration</title>
            <link>http://www.medworm.com/index.php?rid=4901306&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh046672622247l25%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Transmembrane-4-L-six-family-1 (TM4SF1) is a tetraspanin-like membrane protein that is highly and selectively expressed by
 cultured endothelial cells (EC) and, in vivo, by EC lining angiogenic tumor blood vessels. TM4SF1 is necessary for the formation
 of unusually long (up to a 50&amp;nbsp;μm), thin (~100–300&amp;nbsp;nm wide), F-actin-poor EC cell projections that we term ‘nanopodia’. Immunostaining
 of nanopodia at both the light and electron microsopic levels localized TM4SF1 in a regularly spaced, banded pattern, forming
 TM4FS1-enriched domains. Live cell imaging of GFP-transduced HUVEC demonstrated that EC project nanopodia as they migrate
 and interact with neighboring cells. When TM4SF1 mRNA levels in EC were increased from the normal ~90 mRNA copies/cell to
 ~...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4901306</comments>
            <pubDate>Mon, 30 May 2011 17:13:42 +0100</pubDate>
            <guid isPermaLink="false">4901306</guid>        </item>
        <item>
            <title>A note of thanks</title>
            <link>http://www.medworm.com/index.php?rid=4852319&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb1h3878066731hrq%2F</link>
            <description>Content Type Journal ArticlePages 1-2DOI 10.1007/s10456-011-9216-2Authors
		Joyce Bischoff, Boston, MA, USAArjan W. Griffioen, Angiogenesis Laboratory, Department of Medical Oncology, VUMC – Cancer Center Amsterdam, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands
	

	
		Journal AngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4852319</comments>
            <pubDate>Wed, 18 May 2011 18:16:54 +0100</pubDate>
            <guid isPermaLink="false">4852319</guid>        </item>
        <item>
            <title>Taurine: a novel tumor marker for enhanced detection of breast cancer among female patients</title>
            <link>http://www.medworm.com/index.php?rid=4811969&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F222379238126635j%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;It is suggested that assessment of taurine level in sera of patients with high risk for breast cancer are of great value in
 the early diagnosis of malignant changes in the breast.
 
 
 
 
	Content Type Journal ArticlePages 1-10DOI 10.1007/s10456-011-9215-3Authors
		I. M. El Agouza, Faculty of Science, Cairo University, Cairo, EgyptS. S. Eissa, National Cancer Institute, Cairo University, Cairo, EgyptM. M. El Houseini, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, EgyptDalia E. El-Nashar, National Center for Radiation Research and Technology (NCRRT), Atomic Energy Authority, Cairo, EgyptO. M. Abd El Hameed, BMES Department, High Institute of Engineering, Shorouk-Academy, Cairo, Egypt
	

	
		Journal AngiogenesisOnline ISSN 1573-7209Prin...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4811969</comments>
            <pubDate>Sat, 07 May 2011 15:45:02 +0100</pubDate>
            <guid isPermaLink="false">4811969</guid>        </item>
        <item>
            <title>Rho-mediated activation of PI(4)P5K and lipid second messengers is necessary for promotion of angiogenesis by Semaphorin 4D</title>
            <link>http://www.medworm.com/index.php?rid=4794216&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp740132w01x24035%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Phosphatidylinositol 4-phosphate 5-kinase (PI(4)P5K) is a type I lipid kinase that generates the lipid second messenger phospholipid
 phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) and functions downstream of RhoA in actin organization. It is known to play
 an essential role in neurite remodeling, yielding a phenotype identical to that seen in cells treated with Semaphorin 4D (Sema4D),
 a protein that regulates proliferation, adhesion and migration in many different cell types. Plexin-B1, the receptor for Sema4D,
 activates RhoA in order to generate a pro-angiogenic signal in endothelial cells. Therefore, we looked in human umbilical
 vein endothelial cells (HUVEC) to determine if Plexin-B1 exerted control over the cytoskeleton by regulation of PI(4)P5K activity.
 He...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4794216</comments>
            <pubDate>Tue, 03 May 2011 05:57:16 +0100</pubDate>
            <guid isPermaLink="false">4794216</guid>        </item>
        <item>
            <title>Thiodigalactoside inhibits murine cancers by concurrently blocking effects of galectin-1 on immune dysregulation, angiogenesis and protection against oxidative stress</title>
            <link>http://www.medworm.com/index.php?rid=4770689&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fl7775155015m7052%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Cancer cells produce galectin-1 as a tumor promoting protein. Thiodigalactoside (TDG) as a non-metabolised small drug, is
 shown to suppress tumor growth by inhibiting multiple cancer enhancing activities of galectin-1, including immune cell dysregulation,
 angiogenesis and protection against oxidative stress. Thus, using B16F10 melanoma and 4T1 orthotopic breast cancer models,
 intratumoral injection of TDG significantly raised the levels of tumor-infiltrating CD8+ lymphocytes and reduced CD31+ endothelial cell content, reducing tumor growth. TDG treatment of tumors in Balb/c nude mice (defective in T cell immunity)
 reduced angiogenesis and slowed tumor growth by a third less than in immunocompetent mice. Knocking down galectin-1 expression
 (G1KD) in both cancer cell...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4770689</comments>
            <pubDate>Tue, 26 Apr 2011 15:46:54 +0100</pubDate>
            <guid isPermaLink="false">4770689</guid>        </item>
        <item>
            <title>Cyclic GMP protects endothelial progenitors from oxidative stress</title>
            <link>http://www.medworm.com/index.php?rid=4744640&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F5467181q75q88014%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Endothelial progenitor cells (EPCs) play a critical role in the repair of damaged blood vessels and/or in the growth of new
 ones in ischemic tissues. Elevated levels of oxygen radicals, which accumulate in the ischemic tissue, could compromise the
 angiogenic potential of EPCs. To determine if oxidative stress alters the angiogenic response of EPCs and to identify possible
 cellular targets that protect EPCs from the damaging effects of oxidative stress, we have investigated vascular development
 in embryonic bodies (EBs) under hyperoxic conditions. Murine EBs at differentiaton day 2 were cultured for 3&amp;nbsp;days under normoxic
 (21% O2) or hyperoxic (60% O2) conditions. Hyperoxic EBs showed a moderate reduction in Pecam-1, Vegfr-2, eNOS and Tie2 mRNA levels compared t...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4744640</comments>
            <pubDate>Sat, 16 Apr 2011 15:57:35 +0100</pubDate>
            <guid isPermaLink="false">4744640</guid>        </item>
        <item>
            <title>Anti-angiogenic effects of purine inhibitors of cyclin dependent kinases</title>
            <link>http://www.medworm.com/index.php?rid=4722975&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F88340n2h2702x68m%2F</link>
            <description>This study provides first information on how to modify roscovitine
 to develop Cdk inhibitors with increased antiangiogenic activity and suggests the application of existing and the development
 of new Cdk inhibitors to inhibit both, cancer cell proliferation and angiogenesis.
 
 
	Content Type Journal ArticlePages 1-11DOI 10.1007/s10456-011-9212-6Authors
		Johanna Liebl, Department of Pharmacy, Center for Drug Research, Ludwig Maximilians University, Butenandtstr. 5-13, 81377 Munich, GermanyVladimir Krystof, Laboratory of Growth Regulators, Faculty of Science, Palacky University and Institute of Experimental Botany AS CR, 78371 Olomouc, Czech RepublicGyörgy Vereb, Medical and Health Science Centre, Department of Biophysics and Cell Biology, University of Debrecen, 4032 Debrecen, HungaryL...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4722975</comments>
            <pubDate>Tue, 12 Apr 2011 21:37:16 +0100</pubDate>
            <guid isPermaLink="false">4722975</guid>        </item>
        <item>
            <title>Effect of MDM2 and vascular endothelial growth factor inhibition on tumor angiogenesis and metastasis in neuroblastoma</title>
            <link>http://www.medworm.com/index.php?rid=4722976&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fn78213x4g7334824%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Neuroblastoma is the most common pediatric abdominal tumor and principally a p53 wild-type, highly vascular, aggressive tumor,
 with limited response to anti-VEGF therapies alone. MDM2 is a key inhibitor of p53 and a positive activator of hypoxia-inducible
 factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) activity with an important role in neuroblastoma pathogenesis.
 We hypothesized that concurrent inhibition of both MDM2 and VEGF signaling would have cooperative anti-tumor effects, potentiating
 anti-angiogenic strategies for neuroblastoma and other p53 wild-type tumors. We orthotopically implanted SH-SY5Y neuroblastoma
 cells into nude mice (n&amp;nbsp;=&amp;nbsp;40) and treated as follows: control, bevacizumab, Nutlin-3a, combination of bevacizumab plus Nu...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4722976</comments>
            <pubDate>Tue, 12 Apr 2011 06:54:49 +0100</pubDate>
            <guid isPermaLink="false">4722976</guid>        </item>
        <item>
            <title>Potent and sustained inhibition of HIF-1α and downstream genes by a polyethyleneglycol-SN38 conjugate, EZN-2208, results in anti-angiogenic effects</title>
            <link>http://www.medworm.com/index.php?rid=4669564&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft68151n6145q23w3%2F</link>
            <description>In this report, the ability of PEG-SN38 to down-regulate
 HIF-1α and its downstream targets, in a more potent, sustained manner compared with CPT-11 was examined. To do so, U251 glioma
 xenografts that stably expressed a hypoxia response element-dependent luciferase reporter gene were implanted in mice. After
 treatment it was found that EZN-2208 induced potent, sustained HIF-1α down-regulation (37% at 48&amp;nbsp;h and 83% at 120&amp;nbsp;h) in the
 tumors, whereas CPT-11 caused only minor, transient HIF-1α down-regulation. In addition, EZN-2208 down-regulated mRNA levels
 of HIF-1α targeted genes (MMP2, VEGF1, Glut1, Glut3 and TGFβ1). Further, western blot analyses of xenograft tumors demonstrated
 that EZN-2208 had significantly more effect than CPT-11 in down-regulating HIF-1α, VEGF, Glu...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4669564</comments>
            <pubDate>Thu, 31 Mar 2011 07:21:27 +0100</pubDate>
            <guid isPermaLink="false">4669564</guid>        </item>
        <item>
            <title>Neutrophil granulocyte derived MMP-9 is a VEGF independent functional component of the angiogenic switch in pancreatic ductal adenocarcinoma</title>
            <link>http://www.medworm.com/index.php?rid=4641703&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr32r858648133183%2F</link>
            <description>Conclusions/significance&amp;nbsp;&amp;nbsp;PMN derived MMP-9 acts as a potent, direct and VEGF independent angiogenic factor in the context of PDAC. MMP-9 inhibition
 is as effective as VEGF inhibition. Targeting MMP-9 in addition to VEGF is therefore likely to be important for successful
 anti-angiogenic treatment in pancreatic cancer.
 
 
 
 
	Content Type Journal ArticlePages 1-9DOI 10.1007/s10456-011-9207-3Authors
		Dirk Bausch, Department of General and Visceral Surgery, University of Freiburg, Hugstetter Str. 55, 79106 Freiburg, GermanyThomas Pausch, Klinik für Allgemein, Viszeral- und Transplantationschirurgie, Universität Heidelberg, Im Neuenheimer Feld 110, 69120 Heidelberg, GermanyTobias Krauss, Radiologische Universitätsklinik Freiburg i. Br., Hugstetter Str. 55, 79106 Freiburg i. B...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4641703</comments>
            <pubDate>Fri, 25 Mar 2011 18:51:57 +0100</pubDate>
            <guid isPermaLink="false">4641703</guid>        </item>
        <item>
            <title>Angiogenesis as a therapeutic target in arthritis in 2011: learning the lessons of the colorectal cancer experience</title>
            <link>http://www.medworm.com/index.php?rid=4635892&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F7230518910204753%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The paradigm of a therapy aimed at inhibiting the formation of blood vessels, which would consequentially deprive cells and
 tissues of oxygen and nutrients, was born from the concept pioneered by the late Judah Folkman that blood vessel formation
 is central to the progression and maintenance of diseases which involve cellular metabolism and tissue expansion, and cancer
 in particular. The prototype targeted angiogenesis inhibitor anti-vascular endothelial growth factor (VEGF) antibody bevacizumab
 was approved in 2004 for colorectal cancer, and has since been approved for other cancers. Rheumatoid arthritis (RA) is a
 chronic inflammatory disease, during which inflamed tissue invades and destroys cartilage and bone. The tissue expansion,
 invasion, expression of cytok...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4635892</comments>
            <pubDate>Tue, 22 Mar 2011 18:09:22 +0100</pubDate>
            <guid isPermaLink="false">4635892</guid>        </item>
        <item>
            <title>Inhibition of aldose reductase prevents angiogenesis in vitro and in vivo</title>
            <link>http://www.medworm.com/index.php?rid=4610209&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ftu0m67h86237m711%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;We have recently shown that aldose reductase (AR, EC 1.1.1.21) a nicotinamide adenine dinucleotide phosphate-dependent aldo–keto
 reductase, known to be involved in oxidative stress-signaling, prevents human colon cancer cell growth in culture as well
 as in nude mice xenografts. Inhibition of AR also prevents azoxymethane-induced aberrant crypt foci formation in mice. In
 order to understand the chemopreventive mechanism(s) of AR inhibition in colon cancer, we have investigated the role of AR
 in the mediation of angiogenic signals in vitro and in vivo models. Our results show that inhibition of AR significantly prevented
 the VEGF- and FGF -induced proliferation and expression of proliferative marker Ki67 in the human umbilical vein endothelial
 cells (HUVEC). Furth...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4610209</comments>
            <pubDate>Wed, 16 Mar 2011 12:02:14 +0100</pubDate>
            <guid isPermaLink="false">4610209</guid>        </item>
        <item>
            <title>Techniques of assessing hypoxia at the bench and bedside</title>
            <link>http://www.medworm.com/index.php?rid=4494445&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj158172p170782w2%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Tissues require an adequate supply of oxygen in order to maintain normal cell function. Low oxygen tension (hypoxia) is characteristic
 of a number of conditions, including cancer, atherosclerosis, rheumatoid arthritis, critical limb ischaemia, peripheral vascular
 disease, and ischaemic heart disease. Tissue hypoxia is found in tumours, atherosclerotic plaque, and ischaemic myocardium.
 There is a growing interest in methods to detect and assess hypoxia, given that hypoxia is important in the progression of
 these diseases. Hypoxia can be assessed at the level of the whole organ, tissue, or cell, using both invasive and non-invasive
 methods, and by a range of immunohistochemical, biochemical, or imaging techniques. This review describes and critiques current
 methods ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4494445</comments>
            <pubDate>Wed, 16 Feb 2011 06:55:14 +0100</pubDate>
            <guid isPermaLink="false">4494445</guid>        </item>
        <item>
            <title>The natural compound n-butylidenephthalide derived from the volatile oil of Radix Angelica sinensis inhibits angiogenesis in vitro and in vivo</title>
            <link>http://www.medworm.com/index.php?rid=4494444&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F34824m1636842330%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;
 Radix Angelica sinensis is a Chinese medicinal herb that has been used extensively in the East for the treatment of cardiovascular diseases (CVDs).
 Angiogenesis plays an important role in the pathogenesis of CVDs. We hypothesized that Radix A. sinensis may contain angiogenesis modulators. In the current study, we investigated the effects of a volatile oil of Radix A. sinensis (VOAS) and n-butylidenephthalide (BP), one of the bioactive components in VOAS, on angiogenesis in vitro and in vivo. The results suggested
 that VOAS exerted anti-angiogenic effects by inhibiting human umbilical vein endothelial cell proliferation, migration and
 capillary-like tube formation on Matrigel. BP was also shown to be anti-angiogenic and its mechanisms were through inhibition
 of cel...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4494444</comments>
            <pubDate>Wed, 16 Feb 2011 06:55:14 +0100</pubDate>
            <guid isPermaLink="false">4494444</guid>        </item>
        <item>
            <title>Meeting abstracts of the 4th international meeting on angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=4488798&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fa287656531w32112%2F</link>
            <description>Content Type Journal ArticlePages 1-47DOI 10.1007/s10456-011-9203-7

	
		Journal AngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4488798</comments>
            <pubDate>Mon, 14 Feb 2011 07:10:22 +0100</pubDate>
            <guid isPermaLink="false">4488798</guid>        </item>
        <item>
            <title>VEGF masks BNIP3-mediated apoptosis of hypoxic endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=4488799&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F0h08l81144007q31%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Hypoxia results in the apoptotic death of myocytes, neurons, and epithelial cells, through the actions of Bcl-2 and Nineteen
 kilodalton Interacting Protein-3 (BNIP3). On the contrary, endothelial cells are especially adept at surviving conditions
 of oxygen deprivation via up-regulation of vascular endothelial growth factor (VEGF) the most potent endothelial survival
 factor. Both VEGF and BNIP3 expression are transcriptionally regulated by hypoxia inducible factor and may antagonize each
 other’s affects in endothelial cells (ECs). Since factors that promote and inhibit apoptosis may be expressed at the same
 time in endothelial cells under hypoxic conditions, we decided to investigate whether VEGF and BNIP3 have opposing actions
 in endothelial cells. Human microva...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4488799</comments>
            <pubDate>Mon, 14 Feb 2011 06:50:04 +0100</pubDate>
            <guid isPermaLink="false">4488799</guid>        </item>
        <item>
            <title>GSK-3β: a signaling pathway node modulating neural stem cell and endothelial cell interactions</title>
            <link>http://www.medworm.com/index.php?rid=4404935&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F121432n5l72m1183%2F</link>
            <description>In this report we demonstrate GSK-3β’s role as a signaling node in
 two mouse strains (C57BL/6, which have been found to respond to and recover from a hypoxic insult from P3 to P11 poorly and
 CD-1, which have been found to respond to and recover from a hypoxic insult from P3 to P11 well both in vivo and in vitro)
 which mimic the wide range of responsiveness to hypoxic insult observed in the very low birth weight premature infant population.
 Differences in levels of neural stem cell and microvascular endothelial cell GSK-3β activation, β-catenin serine phosphorylation,
 HIF-1α and 2α, BDNF, SDF-1 and VEGF, β-III-tubulin and cleaved notch-1 expression in C57BL/6 and CD-1 subventricular zone
 tissues, and cultured NSC and BEC were noted. Specifically, CD1 pups, SVZ tissues and isol...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4404935</comments>
            <pubDate>Fri, 21 Jan 2011 15:24:35 +0100</pubDate>
            <guid isPermaLink="false">4404935</guid>        </item>
        <item>
            <title>High-resolution mass spectrometric analysis of the secretome from mouse lung endothelial progenitor cells</title>
            <link>http://www.medworm.com/index.php?rid=4355305&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh84q173885123077%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Recently, we isolated and characterized resident endothelial progenitor cells from the lungs of adult mice. These cells have
 a high proliferation potential, are not transformed and can differentiate into blood- and lymph-vascular endothelial cells
 under in vitro and in vivo conditions. Here we studied the secretome of these cells by nanoflow liquid chromatographic mass
 spectrometry (LC–MS). For analysis, 3-day conditioned serum-free media were used. We found 133 proteins belonging to the categories
 of membrane-bound or secreted proteins. Thereby, several of the membrane-bound proteins also existed as released variants.
 Thirty-five proteins from this group are well known as endothelial cell- or angiogenesis-related proteins. The MS analysis
 of the secretome was s...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4355305</comments>
            <pubDate>Fri, 14 Jan 2011 14:17:49 +0100</pubDate>
            <guid isPermaLink="false">4355305</guid>        </item>
        <item>
            <title>Multi-parametric assessment of the anti-angiogenic effects of liposomal glucocorticoids</title>
            <link>http://www.medworm.com/index.php?rid=4342293&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh81375l6112j468h%2F</link>
            <description>In this study, we determined the anti-angiogenic activity of a single dose of liposomal prednisolone phosphate (PLP-L), by
 monitoring tumor vascular function and viability over a period of one week. C57BL/6 mice were inoculated subcutaneously with
 B16F10 melanoma cells. Six animals were PLP-L-treated and six served as control. Tumor tissue and vascular function were probed
 using MRI before and at three timepoints after treatment. DCE-MRI was used to determine Ktrans, ve, time-to-peak, initial slope and the fraction of non-enhancing pixels, complemented with immunohistochemistry. The apparent
 diffusion coefficient (ADC), T2 and tumor size were assessed with MRI as well. PLP-L treatment resulted in smaller tumors and caused a significant drop in
 Ktrans 48&amp;nbsp;h post-treatment, which wa...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342293</comments>
            <pubDate>Tue, 11 Jan 2011 18:03:20 +0100</pubDate>
            <guid isPermaLink="false">4342293</guid>        </item>
        <item>
            <title>Immunohistochemical expression of VEGF predicts response to platinum based chemotherapy in patients with epithelial ovarian cancer</title>
            <link>http://www.medworm.com/index.php?rid=4342294&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fjxj74616k8q27k85%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;We demonstrated that tumours of patients with platinum resistant EOC exhibit higher levels of VEGF expression compared to
 the platinum sensitive group. VEGF in EOC, may be of clinical and therapeutic relevance and suggests a role for first line
 anti-angiogenic therapy.
 
 
 
 
	Content Type Journal ArticlePages 1-7DOI 10.1007/s10456-010-9199-4Authors
		G. K. Siddiqui, Department of Obstetrivs and Gynaecology, Royal Free and University College Medical School, London, UKA. B. Maclean, Department of Obstetrivs and Gynaecology, Royal Free and University College Medical School, London, UKK. Elmasry, Division of Gynaecological Oncology, Tawam Hospital in affiliation with John Hopkins, Al Ain, United Arab EmiratesA. Wong te Fong, Department of Obstetrivs and Gynaecology, R...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342294</comments>
            <pubDate>Mon, 10 Jan 2011 16:15:16 +0100</pubDate>
            <guid isPermaLink="false">4342294</guid>        </item>
        <item>
            <title>Vascular endothelial growth inhibitor (VEGI; TNFSF15) inhibits bone marrow-derived endothelial progenitor cell incorporation into Lewis lung carcinoma tumors</title>
            <link>http://www.medworm.com/index.php?rid=4301973&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr0u4v3463670664h%2F</link>
            <description>We report here that treatment of tumor bearing
 mice with recombinant VEGI leads to a significantly decreased population of BM-derived EPC in the tumors. We transplanted
 whole bone marrow from green fluorescent protein (GFP) transgenic mice into C57BL/6 recipient mice, which were then inoculated
 with Lewis lung carcinoma (LLC) cells. Intraperitoneal injection of recombinant VEGI led to significant inhibition of tumor
 growth and decrease of vasculature density compared to vehicle-treated mice. Tumor implantation yielded a decrease of BM-derived
 EPC in the peripheral blood, while VEGI-treatment resulted in an initial delay of such decrease. Analysis of the whole bone
 marrow showed a decrease of Lin−-c-Kit+-Sca-1+ hematopoietic stem cell (HSC) population in tumor bearing mice; however,...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4301973</comments>
            <pubDate>Tue, 28 Dec 2010 15:34:51 +0100</pubDate>
            <guid isPermaLink="false">4301973</guid>        </item>
        <item>
            <title>Antiangiogenic tyrosine kinase inhibition related gastrointestinal perforations: a case report and literature review</title>
            <link>http://www.medworm.com/index.php?rid=4301974&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F1352800165087174%2F</link>
            <description>In conclusion,
 while clinical awareness that antiangiogenic treatment can cause GI perforations is critical for current medical practice,
 it is also very important to get more insight in its underlying mechanisms so that this life-threatening complication may
 be prevented in the near future.
 
 
	Content Type Journal ArticleDOI 10.1007/s10456-010-9197-6Authors
		Maudy Walraven, Department of Medical Oncology, VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, The NetherlandsPetronella O. Witteveen, Department of Medical Oncology, University Medical Center Utrecht, Utrecht, The NetherlandsMartijn P. J. Lolkema, Department of Medical Oncology, University Medical Center Utrecht, Utrecht, The NetherlandsR. van Hillegersberg, Department of Surgery, University Medical Center ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4301974</comments>
            <pubDate>Tue, 28 Dec 2010 15:34:49 +0100</pubDate>
            <guid isPermaLink="false">4301974</guid>        </item>
        <item>
            <title>Bone marrow cells participate in tumor vessel formation that supports the growth of Ewing’s sarcoma in the lung</title>
            <link>http://www.medworm.com/index.php?rid=4288347&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx016v64281886064%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;An MHC-mismatch bone marrow (BM) transplant Ewing’s sarcoma mouse model was used to investigate whether BM cells participate
 in the vessel formation that support Ewing’s sarcoma lung metastasis. BM cells from H-2Kb/d donor mice were transplanted into sublethally irradiated H-2Kd recipient mice. Donor BM cells were identified using the H-2Kb marker. Engraftment was confirmed by identifying the H-2Kb IL-1β-type specific polymorphism. After engraftment highly lung metastatic TC71-PM4 cells were injected intravenously. Mice
 were sacrificed 10&amp;nbsp;weeks after tumor cell injection. Hematoxylin-and-eosin staining was performed to identify lung metastatic
 foci. These tumors were then evaluated using immunohistochemical analysis. H-2Kb-positive cells were found in lung ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4288347</comments>
            <pubDate>Thu, 23 Dec 2010 17:49:42 +0100</pubDate>
            <guid isPermaLink="false">4288347</guid>        </item>
        <item>
            <title>SR16388: a steroidal antiangiogenic agent with potent inhibitory effect on tumor growth in vivo</title>
            <link>http://www.medworm.com/index.php?rid=4196284&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx545161327v62076%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Angiogenesis is one of the major processes controlling growth and metastasis of tumors. Angiogenesis inhibitors have been
 targeted for the treatment of various cancers for more than 2 decades. We have developed a novel class of steroidal compounds
 aimed at blocking the angiogenic process in cancerous tissues. Our lead compound, SR16388, is a potent antiangiogenic agent
 with binding affinity to estrogen receptor-α (ER-α) and -β (ER-β) at the nanomolar range. This compound inhibited the proliferation
 of human microvascular endothelial cells (HMVEC) and various types of human cancer cells in vitro. SR16388 inhibited embryonic
 angiogenesis as measured in the chick chorioallantoic membrane (CAM) assay. The blood vessel density in the CAM was greatly
 reduced after t...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4196284</comments>
            <pubDate>Sat, 20 Nov 2010 17:51:01 +0100</pubDate>
            <guid isPermaLink="false">4196284</guid>        </item>
        <item>
            <title>Mesenchymal stem cells from adipose and bone marrow promote angiogenesis via distinct cytokine and protease expression mechanisms</title>
            <link>http://www.medworm.com/index.php?rid=4196283&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F7p62p154p378474u%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Using a fibrin-based angiogenesis model, we have established that there is no canonical mechanism used by endothelial cells
 (ECs) to degrade the surrounding extracellular matrix (ECM), but rather the set of proteases used is dependent on the mural
 cells providing the angiogenic cues. Mesenchymal stem cells (MSCs) originating from different tissues, which are thought to
 be phenotypically similar, promote angiogenesis through distinct mechanisms. Specifically, adipose-derived stem cells (ASCs)
 promote utilization of the plasminogen activator-plasmin axis by ECs as the primary means of vessel invasion and elongation
 in fibrin. Matrix metalloproteinases (MMPs) serve a purpose in regulating capillary diameter and possibly in stabilizing the
 nascent vessels. These prote...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4196283</comments>
            <pubDate>Sat, 20 Nov 2010 17:51:01 +0100</pubDate>
            <guid isPermaLink="false">4196283</guid>        </item>
        <item>
            <title>Gold nanoparticles inhibit vascular endothelial growth factor-induced angiogenesis and vascular permeability via Src dependent pathway in retinal endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=4149835&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F36070m6m480t0533%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The purpose of this study was to investigate the effect of gold nanoparticles on the signaling cascade related to angiogenesis
 and vascular permeability induced by Vascular Endothelial Growth Factor (VEGF) in Bovine retinal endothelial cells (BRECs).
 The effect of VEGF and gold nanoparticles on cell viability, migration and tubule formation was assessed. PP2 (Src Tyrosine
 Kinase inhibitor) was used as the positive control and the inhibitor assay was performed to compare the effect of AuNPs on
 VEGF induced angiogenesis. The transient transfection assay was performed to study the VEGFR2/Src activity during experimental
 conditions and was confirmed using western blot analysis. Treatment of BRECs with VEGF significantly increased the cell proliferation,
 migration and ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4149835</comments>
            <pubDate>Mon, 08 Nov 2010 19:18:42 +0100</pubDate>
            <guid isPermaLink="false">4149835</guid>        </item>
        <item>
            <title>Treprostinil increases the number and angiogenic potential of endothelial progenitor cells in children with pulmonary hypertension</title>
            <link>http://www.medworm.com/index.php?rid=4142466&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fd64645v722626531%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;ECFC may partly mediate the clinical benefits of prostanoids in pulmonary arterial hypertension.
 
 
 
	Content Type Journal ArticleDOI 10.1007/s10456-010-9192-yAuthors
		David M. Smadja, Université Paris Descartes, Paris, FranceLaetitia Mauge, Université Paris Descartes, Paris, FrancePascale Gaussem, Université Paris Descartes, Paris, FranceClément d’Audigier, Université Paris Descartes, Paris, FranceDominique Israel-Biet, Université Paris Descartes, Paris, FranceDavid S. Celermajer, Sydney Medical School, University of Sydney, Sydney, NSW 2006, AustraliaDamien Bonnet, Université Paris Descartes, Paris, FranceMarilyne Lévy, Université Paris Descartes, Paris, France
	

	
		Journal AngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4142466</comments>
            <pubDate>Wed, 03 Nov 2010 17:03:42 +0100</pubDate>
            <guid isPermaLink="false">4142466</guid>        </item>
        <item>
            <title>Placental growth factor neutralising antibodies give limited anti-angiogenic effects in an in vitro organotypic angiogenesis model</title>
            <link>http://www.medworm.com/index.php?rid=4096024&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F9032442741223864%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Vascular Endothelial Growth Factor Receptor (VEGFR) mediated signalling drives angiogenesis. This is predominantly attributed
 to the activity of VEGFR-2 following binding of VEGF-A. Whether other members of the VEGFR and ligand families such as VEGFR-1
 and its ligand Placental Growth Factor (PlGF) can also contribute to developmental and pathological angiogenesis is less clear.
 We explored the function of PlGF in VEGF-A dependent angiogenesis using an in vitro co-culture assay in which endothelial
 cells are cultured on a fibroblast feeder layer. In the presence of 2% FS MCDB media (containing limited growth factors) in
 vitro endothelial tube formation is driven by endogenous angiogenic stimuli which are produced by the fibroblast and endothelial
 cells. Under these...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4096024</comments>
            <pubDate>Sat, 16 Oct 2010 09:04:52 +0100</pubDate>
            <guid isPermaLink="false">4096024</guid>        </item>
        <item>
            <title>Anti-angiogenic effects of resveratrol mediated by decreased VEGF and increased TSP1 expression in melanoma-endothelial cell co-culture</title>
            <link>http://www.medworm.com/index.php?rid=4044365&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fn1162128202m0756%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Resveratrol, a naturally occurring polyphenol, has been reported to be an anti-tumor and chemopreventive agent. Recent data
 show that it may also exert anti-angiogenic effects. We hypothesized that the anti-angiogenic activity of resveratrol may
 be caused by modulation of tumor cell release of thrombospondin-1 (TSP1) and vascular endothelial growth factor (VEGF) into
 the extracellular matrix, leading to vascular endothelial cell (VEC) apoptosis. We therefore evaluated the effects of resveratrol
 on melanoma cell lines co-cultured with vascular endothelial cells in monolayer and in three dimensional spheroids. We found
 that resveratrol stimulated isolated VEC proliferation, while it caused growth inhibition of VECs grown with melanoma cells
 in three-dimensional co-c...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4044365</comments>
            <pubDate>Wed, 06 Oct 2010 16:45:19 +0100</pubDate>
            <guid isPermaLink="false">4044365</guid>        </item>
        <item>
            <title>Targeting NF-κB in infantile hemangioma-derived stem cells reduces VEGF-A expression</title>
            <link>http://www.medworm.com/index.php?rid=4002662&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F34544g6260r25038%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;We demonstrate expression of NF-κB target genes in proliferating IH. In addition, we show that the expression of several pro-angiogenic
 factors in HemSCs, and in particular&amp;nbsp;VEGF–A, is regulated by NF-B activity.
 
 
 
 
	Content Type Journal ArticleDOI 10.1007/s10456-010-9189-6Authors
		Shoshana Greenberger, Vascular Biology Program and Department of Surgery, Children’s Hospital Boston and Harvard Medical School, Boston, MA 02115, USAIrit Adini, Vascular Biology Program and Department of Surgery, Children’s Hospital Boston and Harvard Medical School, Boston, MA 02115, USAElisa Boscolo, Vascular Biology Program and Department of Surgery, Children’s Hospital Boston and Harvard Medical School, Boston, MA 02115, USAJohn B. Mulliken, Department of Plastic S...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4002662</comments>
            <pubDate>Fri, 24 Sep 2010 17:07:27 +0100</pubDate>
            <guid isPermaLink="false">4002662</guid>        </item>
        <item>
            <title>Comparative analysis of angiogenic gene expression in normal and impaired wound healing in diabetic mice: effects of extracorporeal shock wave therapy</title>
            <link>http://www.medworm.com/index.php?rid=3981887&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw83h46n6449810q0%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Impaired wound healing is a persistent clinical problem which has been treated with mixed results. Studies aimed at elucidating
 the mechanism of impaired wound healing have focused on small cohorts of genes which leave an incomplete picture of the wound
 healing process. We aimed to investigate impaired wound healing via a comprehensive panel of angiogenic/inflammation-related
 genes and wound closure kinetics with and without the application of extracorporeal shock wave therapy (ESWT), which has been
 demonstrated to improve wound healing. Full-thickness skin from the dorsal surface of “normal” (BALB/c) and “impaired” (db
 +/db
 +) mice was excised, and wound margin tissue was harvested 2, 7, and 10&amp;nbsp;days post injury. A separate, but identical wound model
...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3981887</comments>
            <pubDate>Fri, 17 Sep 2010 06:47:10 +0100</pubDate>
            <guid isPermaLink="false">3981887</guid>        </item>
        <item>
            <title>The impact of EPLINα (Epithelial protein lost in neoplasm) on endothelial cells, angiogenesis and tumorigenesis</title>
            <link>http://www.medworm.com/index.php?rid=3981888&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv7k0382272781u15%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;EPLINα over-expression can regulate HECV cell motility, matrix adhesion and tubule formation in vitro and slow in vivo tumour
 formation, suggesting an anti-angiogenic role for EPLINα. Extracellular signal-regulated kinase (ERK) also appears to be linked
 to the ability of EPLINα to inhibit tubule formation in vitro.
 
 
 
 
	Content Type Journal ArticleDOI 10.1007/s10456-010-9188-7Authors
		Andrew J. Sanders, Metastasis and Angiogenesis Research Group, Cardiff University School of Medicine, Cardiff, CF14 4XN UKLin Ye, Metastasis and Angiogenesis Research Group, Cardiff University School of Medicine, Cardiff, CF14 4XN UKMalcolm D. Mason, Department of Clinical Oncology, Cardiff University School of Medicine, Cardiff, UKWen G. Jiang, Metastasis and Angiogenesis Res...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3981888</comments>
            <pubDate>Fri, 17 Sep 2010 06:47:09 +0100</pubDate>
            <guid isPermaLink="false">3981888</guid>        </item>
        <item>
            <title>Vascular regrowth following photodynamic therapy in the chicken embryo chorioallantoic membrane</title>
            <link>http://www.medworm.com/index.php?rid=3980188&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F6347135760502201%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Photodynamic therapy (PDT) induces damage to the endothelium, which can lead to increased vascular permeability and, under
 intensive PDT conditions, even to platelet aggregation, vasoconstriction, and blood flow stasis. Eventually, ischemia, hypoxia,
 and inflammation can occur, resulting in angiogenesis. We studied the sequence of the vascular events after Visudyne®-PDT in the chicken chorioallantoic membrane (CAM) at day 11 of development. Using epi-fluorescence microscopy, we monitored
 the regrowth of capillaries in the PDT treated area. Immediately after irradiation, the treatment resulted in blood flow arrest.
 And 24&amp;nbsp;h post PDT, sprouting of new blood vessels was observed at the edge of the PDT zone. Neovessels looping out from the
 edge of the PDT zone ga...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3980188</comments>
            <pubDate>Tue, 14 Sep 2010 18:10:26 +0100</pubDate>
            <guid isPermaLink="false">3980188</guid>        </item>
        <item>
            <title>Moderate GSK-3β inhibition improves neovascular architecture, reduces vascular leakage, and reduces retinal hypoxia in a model of ischemic retinopathy</title>
            <link>http://www.medworm.com/index.php?rid=3932633&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh0l577287321g082%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In ischemic retinopathies, unrelieved hypoxia induces the formation of architecturally abnormal, leaky blood vessels that
 damage retina and ultimately can cause blindness. Because these newly formed blood vessels are functionally defective, they
 fail to alleviate underlying hypoxia, resulting in more pathological neovascularization and more damage to retina. With an
 established model of ischemic retinopathy, we investigated inhibition of glycogen synthase kinase-3β (GSK-3β) as a means for
 improving the architecture and functionality of pathological blood vessels in retina. In vitro, hypoxia increased GSK-3β activity
 in retinal endothelial cells, reduced β-catenin, and correspondingly impaired integrity of cell/cell junctions. Conversely,
 GSK-3β inhibitors res...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3932633</comments>
            <pubDate>Thu, 02 Sep 2010 06:53:55 +0100</pubDate>
            <guid isPermaLink="false">3932633</guid>        </item>
        <item>
            <title>The small molecule specific EphB4 kinase inhibitor NVP-BHG712 inhibits VEGF driven angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=3920111&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fhw2k177057756700%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;EphB4 and its cognitive ligand ephrinB2 play an important role in embryonic vessel development and vascular remodeling. In
 addition, several reports suggest that this receptor ligand pair is also involved in pathologic vessel formation in adults
 including tumor angiogenesis. Eph/ephrin signaling is a complex phenomena characterized by receptor forward signaling through
 the tyrosine kinase of the receptor and ephrin reverse signaling through various protein–protein interaction domains and phosphorylation
 motifs of the ephrin ligands. Therefore, interfering with EphR/ephrin signaling by the means of targeted gene ablation, soluble
 receptors, dominant negative mutants or antisense molecules often does not allow to discriminate between inhibition of Eph/ephrin
 forwa...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3920111</comments>
            <pubDate>Sat, 28 Aug 2010 17:05:22 +0100</pubDate>
            <guid isPermaLink="false">3920111</guid>        </item>
        <item>
            <title>Minimally invasive assessment of tumor angiogenesis by fine needle aspiration and flow cytometry</title>
            <link>http://www.medworm.com/index.php?rid=3898852&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fn6815m5325l0441t%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The development of a new, less invasive, and more rapidly implemented method of quantifying endothelial cell density in tumors
 could facilitate experimental and clinical studies of angiogenesis. Therefore, we evaluated the utility of tumor fine needle
 aspiration (FNA) coupled with flow cytometry for assessment of tumor angiogenesis. Samples were obtained from cutaneous tumors
 of mice using FNA, then immunostained and assessed by flow cytometry to determine the number of CD31+ endothelial cells. Results of the FNA/flow cytometry technique were compared with quantification of tumor microvessel density
 using immunohistochemistry. The ability of the FNA/cytometry technique to quantify the effects of anti-angiogenic therapy
 and to monitor changes in tumor angiogenesis o...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3898852</comments>
            <pubDate>Mon, 23 Aug 2010 17:58:48 +0100</pubDate>
            <guid isPermaLink="false">3898852</guid>        </item>
        <item>
            <title>Anti-angiogenic potential of small molecular inhibitors of cyclin dependent kinases in vitro</title>
            <link>http://www.medworm.com/index.php?rid=3866756&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F35017772l68250p0%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Small molecular kinase inhibitors are promising novel drugs. Initially, they were designed for the highest possible specificity.
 Recently, this concept has been challenged by multikinase inhibitors, which are clinically more potent. This change of paradigm
 calls for re-examination of already known compounds in different functional contexts. We have compared 6 reported structurally
 different inhibitors of cyclin-dependent kinases (Cdks) regarding their functional effects on endothelial cells (proliferation,
 cell cycle, apoptosis, migration, tube formation), as well as their actions on some kinases (AKT, p38, ERK1/2, c-src, GSK3β).
 Only some of these compounds had anti-angiogenic effects in concentrations up to 10&amp;nbsp;μM (aminopurvalanol, indirubin-3′-monoxime,
...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3866756</comments>
            <pubDate>Thu, 12 Aug 2010 18:44:16 +0100</pubDate>
            <guid isPermaLink="false">3866756</guid>        </item>
        <item>
            <title>The inhibition of autophagy potentiates anti-angiogenic effects of sulforaphane by inducing apoptosis</title>
            <link>http://www.medworm.com/index.php?rid=3861426&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fch00277v42637773%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;Similar to cancer cells, ECs induced autophagy in response to the pro-apoptotic agent, SUL, and the inhibition of autophagy
 potentiated the pro-apoptotic effect. These findings open premises for the use of autophagy inhibitors in combination with
 anti–angiogenic agents.
 
 
 
 
	Content Type Journal ArticleDOI 10.1007/s10456-010-9180-2Authors
		Takeshi Nishikawa, Department of Surgical Oncology, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655 JapanNelson H. Tsuno, Department of Surgical Oncology, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655 JapanYurai Okaji, Department of Transfusion Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, JapanEiji Sunami, Department of Surgical ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3861426</comments>
            <pubDate>Sat, 07 Aug 2010 16:49:01 +0100</pubDate>
            <guid isPermaLink="false">3861426</guid>        </item>
        <item>
            <title>Intravital microscopy in window chambers: a unique tool to study tumor angiogenesis and delivery of nanoparticles</title>
            <link>http://www.medworm.com/index.php?rid=3749670&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm008rl6161366210%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Solid tumor growth is heavily dependant on angiogenesis. Tumor angiogenesis is the result of a complex interplay between tumor
 cells, endothelial cells, and other stromal cells. It has been found to be under strict control of a plethora of molecular
 factors that function as angiogenic up- and down-regulators; nevertheless, the identification of molecular and cellular players
 and their roles in angiogenesis is still ongoing. The microvasculature resulting from tumor angiogenesis lacks hierarchy and
 has a high permeability for macromolecules and nanoparticles, which offers significant potential for nanoparticulate tumor
 imaging and drug delivery platforms. However, improvements in the delivery to poorly vascularized regions and the distribution
 throughout the tumor ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3749670</comments>
            <pubDate>Sat, 10 Jul 2010 06:46:12 +0100</pubDate>
            <guid isPermaLink="false">3749670</guid>        </item>
        <item>
            <title>MCP-1 promotes mural cell recruitment during angiogenesis in the aortic ring model</title>
            <link>http://www.medworm.com/index.php?rid=3694811&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft453841g6348287j%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Rings of rat or mouse aorta embedded in collagen gels produce angiogenic outgrowths in response to the injury of the dissection
 procedure. Aortic outgrowths are composed of branching endothelial tubes and surrounding mural cells. Mural cells emerge following
 endothelial sprouting and gradually increase during the maturation of the neovessels. Treatment of aortic cultures with angiopoietin-1
 (Ang-1), an angiogenic factor implicated in vascular maturation and remodeling, stimulates the mural cell recruitment process.
 Ang-1 induces expression of many cytokines and chemokines including monocyte chemotactic protein-1 (MCP-1). Inhibition of
 p38 MAP kinase, a signaling molecule required for mural cell recruitment, blocks Ang1-induced MCP-1 expression. Recombinant
 MCP-1 d...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3694811</comments>
            <pubDate>Tue, 22 Jun 2010 18:35:11 +0100</pubDate>
            <guid isPermaLink="false">3694811</guid>        </item>
        <item>
            <title>Imaging of angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=3678424&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F5483424821303vv2%2F</link>
            <description>Content Type Journal ArticleCategory Editorial NoteDOI 10.1007/s10456-010-9178-9Authors
		Willem J. M. Mulder, Mount Sinai School of Medicine Translational and Molecular Imaging Institute One Gustave L. Levy Place Box 1234 New York NY USAArjan W. Griffioen, VU University Medical Center Angiogenesis Laboratory, Department of Medical Oncology, VUmc-Cancer Center Amsterdam Amsterdam The Netherlands
	

	
		Journal AngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3678424</comments>
            <pubDate>Fri, 18 Jun 2010 10:36:42 +0100</pubDate>
            <guid isPermaLink="false">3678424</guid>        </item>
        <item>
            <title>Resequencing of the vascular endothelial growth factor promoter reveals haplotype structure and functional diversity</title>
            <link>http://www.medworm.com/index.php?rid=3670891&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F0m5216655p322160%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Our group has previously reported that SNPs in the VEGF promoter are strongly associated with efficacy and toxicity to the
 anti-VEGF antibody bevacizumab in breast cancer. In order to better understand the biologic mechanism for our previously reported
 biomarkers, we embarked on a comprehensive evaluation of genetic variation in the VEGF promoter coupled with a study of its
 intrinsic function. We resequenced 48 Caucasians and 48 African-Americans for the VEGF promoter to identify SNPs and elucidate
 its haplotype structure. We further cloned the haplotypes into reporter constructs and assessed the role of SNPs on promoter
 function in breast cancer cell lines. SNPs that were identified included twenty previously reported SNPs/insertions/deletions,
 one novel SNP, and...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3670891</comments>
            <pubDate>Wed, 16 Jun 2010 07:26:17 +0100</pubDate>
            <guid isPermaLink="false">3670891</guid>        </item>
        <item>
            <title>Quantum dots for multimodal molecular imaging of angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=3670890&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F8kxw5v0008679517%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Quantum dots exhibit unique optical properties for bioimaging purposes. We have previously developed quantum dots with a paramagnetic
 and functionalized coating and have shown their potential for molecular imaging purposes. In the current mini-review we summarize
 the synthesis procedure, the in&amp;nbsp;vitro testing and, importantly, the in vivo application for multimodal molecular imaging of
 tumor angiogenesis.
 
 
	Content Type Journal ArticleCategory Original PaperDOI 10.1007/s10456-010-9177-xAuthors
		Willem J. M. Mulder, Mount Sinai School of Medicine Translational and Molecular Imaging Institute One Gustave L. Levy Place Box 1234 New York NY 10029 USAGustav J. Strijkers, Eindhoven University of Technology Biomedical NMR, Department of Biomedical Engineering Eindho...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3670890</comments>
            <pubDate>Wed, 16 Jun 2010 07:26:17 +0100</pubDate>
            <guid isPermaLink="false">3670890</guid>        </item>
        <item>
            <title>Magnetic resonance imaging of brain angiogenesis after stroke</title>
            <link>http://www.medworm.com/index.php?rid=3670892&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff6222g8745743511%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Stroke is a major cause of mortality and long-term disability worldwide. The initial changes in local perfusion and tissue
 status underlying loss of brain function are increasingly investigated with noninvasive imaging methods. In addition, there
 is a growing interest in imaging of processes that contribute to post-stroke recovery. In this review, we discuss the application
 of magnetic resonance imaging (MRI) to assess the formation of new vessels by angiogenesis, which is hypothesized to participate
 in brain plasticity and functional recovery after stroke. The excellent soft tissue contrast, high spatial and temporal resolution,
 and versatility render MRI particularly suitable to monitor the dynamic processes involved in vascular remodeling after stroke.
 Here we ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3670892</comments>
            <pubDate>Wed, 16 Jun 2010 07:26:16 +0100</pubDate>
            <guid isPermaLink="false">3670892</guid>        </item>
        <item>
            <title>Molecular ultrasound assessment of tumor angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=3670893&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc124333480042043%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Angiogenesis, the growth of new blood vessels, plays a critical role in progression of tumor growth and metastasis, making
 it an attractive target for both cancer imaging and therapy. Several molecular markers, including those that are involved
 in the angiogenesis signaling pathway and those unique to tumor angiogenic vessels, have been identified and can be used as
 targets for molecular imaging of cancer. With the introduction of ultrasound contrast agents that can be targeted to those
 molecular markers, targeted contrast-enhanced ultrasound (molecular ultrasound) imaging has become an attractive imaging modality
 to non-invasively assess tumor angiogenesis at the molecular level. The advantages of molecular ultrasound imaging such as
 high temporal and spatial res...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3670893</comments>
            <pubDate>Mon, 14 Jun 2010 14:08:02 +0100</pubDate>
            <guid isPermaLink="false">3670893</guid>        </item>
        <item>
            <title>Erratum to: Vascular endothelial growth factor and its relationship to the prognosis and treatment of breast, ovarian, and cervical cancer</title>
            <link>http://www.medworm.com/index.php?rid=3655288&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fym7352243j2r498t%2F</link>
            <description>Content Type Journal ArticleCategory ErratumDOI 10.1007/s10456-010-9171-3Authors
		Jennifer Delli Carpini, Memorial Sloan-Kettering Cancer Center Breast Service, Department of Surgery 1275 York Avenue New York NY 10065 USAAmer K. Karam, Memorial Sloan-Kettering Cancer Center Breast Service, Department of Surgery 1275 York Avenue New York NY 10065 USALeslie Montgomery, Memorial Sloan-Kettering Cancer Center Breast Service, Department of Surgery 1275 York Avenue New York NY 10065 USA
	

	
		Journal AngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3655288</comments>
            <pubDate>Thu, 10 Jun 2010 17:40:45 +0100</pubDate>
            <guid isPermaLink="false">3655288</guid>        </item>
        <item>
            <title>Dynamic contrast enhanced (DCE) magnetic resonance imaging (MRI) of atherosclerotic plaque angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=3651910&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fwu17108730x56187%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Atherosclerosis is a progressive systemic disease of the large arteries characterized by the formation of plaques in the vessel
 wall. Despite our knowledge of its pathogenesis, many vulnerable plaques still remain undiagnosed while in their asymptomatic
 phase and manifest for the first time with dramatic clinical events, such as stroke or myocardial infarction. In recent years,
 it is becoming clearer that sudden clinical events do not necessarily correlate with the degree of luminal obstruction caused
 by lesions, but rather with plaque composition. In particular, the degree of plaque inflammation is important in the pathogenesis
 of atherosclerosis and is considered a good marker of high-risk/vulnerable plaques. The presence of inflammatory infiltrate
 and plaque ne...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3651910</comments>
            <pubDate>Mon, 07 Jun 2010 16:14:00 +0100</pubDate>
            <guid isPermaLink="false">3651910</guid>        </item>
        <item>
            <title>Visualizing vascular permeability and lymphatic drainage using labeled serum albumin</title>
            <link>http://www.medworm.com/index.php?rid=3628998&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fq27u43t243gh6444%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;During the early stages of angiogenesis, following stimulation of endothelial cells by vascular endothelial growth factor
 (VEGF), the vascular wall is breached, allowing high molecular weight proteins to leak from the vessels to the interstitial
 space. This hallmark of angiogenesis results in deposition of a provisional matrix, elevation of the interstitial pressure
 and induction of interstitial convection. Albumin, the major plasma protein appears to be an innocent bystander that is significantly
 affected by these changes, and thus can be used as a biomarker for vascular permeability associated with angiogenesis. Traditionally,
 albumin leak in superficial organs was followed by colorimetry or morphometry with the use of albumin binding vital dyes.
 Over the last y...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3628998</comments>
            <pubDate>Fri, 28 May 2010 18:02:48 +0100</pubDate>
            <guid isPermaLink="false">3628998</guid>        </item>
        <item>
            <title>Transplantation of sendai viral angiopoietin-1-modified mesenchymal stem cells for ischemic limb disease</title>
            <link>http://www.medworm.com/index.php?rid=3563354&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy33j2508467q5062%2F</link>
            <description>In this study,
 we infected SeV to the MSCs in vitro; and injected MSCs modified with SeV harboring human angiopoietin-1 gene (SeVhAng-1)
 into the ischemic limb of rats in vivo. We found SeV had high transductive efficiency to the MSCs. Both MSCs and SeVhAng-1-modified
 MSCs improved the blood flow recovery and increased the capillary density of the ischemic limb, compared with the control.
 However, in contrast to MSCs, SeVhAng-1-modified MSCs had a better improvement of blood flow recovery in the ischemic limb.
 We further found the ischemic limb injected with SeVhAng-1-modified MSCs had strong expression of p-Akt, which improved survival
 of MSCs injected into the ischemic limb. This indicated SeVhAng-1 modification enhanced angiogenetic effect of MSCs by both
 angiogenesis and cell pr...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3563354</comments>
            <pubDate>Tue, 11 May 2010 08:12:35 +0100</pubDate>
            <guid isPermaLink="false">3563354</guid>        </item>
        <item>
            <title>‘In vivo’ optical approaches to angiogenesis imaging</title>
            <link>http://www.medworm.com/index.php?rid=3546781&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F693t526x27t42rtk%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In recent years, molecular imaging gained significant importance in biomedical research. Optical imaging developed into a
 modality which enables the visualization and quantification of all kinds of cellular processes and cancerous cell growth in
 small animals. Novel gene reporter mice and cell lines and the development of targeted and cleavable fluorescent “smart” probes
 form a powerful imaging toolbox. The development of systems collecting tomographic bioluminescence and fluorescence data enabled
 even more spatial accuracy and more quantitative measurements. Here we describe various bioluminescent and fluorescent gene
 reporter models and probes that can be used to specifically image and quantify neovascularization or the angiogenic process
 itself.
 
 
	Conten...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3546781</comments>
            <pubDate>Fri, 07 May 2010 08:45:33 +0100</pubDate>
            <guid isPermaLink="false">3546781</guid>        </item>
        <item>
            <title>Theragnostics for tumor and plaque angiogenesis with perfluorocarbon nanoemulsions</title>
            <link>http://www.medworm.com/index.php?rid=3502693&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F00712680170w0r2r%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Molecular imaging agents are extending the potential of noninvasive medical diagnosis from basic gross anatomical descriptions
 to complicated phenotypic characterizations based upon the recognition of unique cell-surface biochemical signatures. Although
 originally the purview of nuclear medicine, “molecular imaging” is now studied in conjunction with all clinically relevant
 imaging modalities. Of the myriad of particles that have emerged as prospective candidates for clinical translation, perfluorocarbon
 nanoparticles offer great potential for combining targeted imaging with drug delivery, much like the “magic bullet” envisioned
 by Paul Ehrlich 100&amp;nbsp;years ago. Perfluorocarbon nanoparticles, once studied in Phase III clinical trials as blood substitutes,...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3502693</comments>
            <pubDate>Thu, 22 Apr 2010 09:12:04 +0100</pubDate>
            <guid isPermaLink="false">3502693</guid>        </item>
        <item>
            <title>Paramagnetic and fluorescent liposomes for target-specific imaging and therapy of tumor angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=3482509&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fq4l502811342182k%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Angiogenesis is essential for tumor growth and metastatic potential and for that reason considered an important target for
 tumor treatment. Noninvasive imaging technologies, capable of visualizing tumor angiogenesis and evaluating the efficacy of
 angiostatic therapies, are therefore becoming increasingly important. Among the various imaging modalities, magnetic resonance
 imaging (MRI) is characterized by a superb spatial resolution and anatomical soft-tissue contrast. Revolutionary advances
 in contrast agent chemistry have delivered versatile angiogenesis-specific molecular MRI contrast agents. In this paper, we
 review recent advances in the preclinical application of paramagnetic and fluorescent liposomes for noninvasive visualization
 of the molecular processes i...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3482509</comments>
            <pubDate>Wed, 14 Apr 2010 06:54:39 +0100</pubDate>
            <guid isPermaLink="false">3482509</guid>        </item>
        <item>
            <title>Non-invasive imaging of angiogenesis in head and neck squamous cell carcinoma</title>
            <link>http://www.medworm.com/index.php?rid=3467201&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc50k6812k30371hx%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Squamous cell carcinoma of the head and neck (HNSCC) is the seventh most common cancer in the United States. Angiogenesis,
 the process by which new blood vessels are formed, is an essential element at the basis of both tumor growth and metastases.
 This review discusses pertinent aspects of the role of imaging modalities in assessing angiogenesis and anti-angiogenic therapy
 in advanced HNSCC.
 
 
	Content Type Journal ArticleDOI 10.1007/s10456-010-9167-zAuthors
		Jacobus F. A. Jansen, Memorial Sloan-Kettering Cancer Center Department of Medical Physics 1275 York Avenue New York NY 10065 USAJason A. Koutcher, Memorial Sloan-Kettering Cancer Center Department of Medical Physics 1275 York Avenue New York NY 10065 USAAmita Shukla-Dave, Memorial Sloan-Kettering Cancer Cent...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3467201</comments>
            <pubDate>Sun, 11 Apr 2010 05:50:59 +0100</pubDate>
            <guid isPermaLink="false">3467201</guid>        </item>
        <item>
            <title>Vascular endothelial growth factor and its relationship to the prognosis and treatment of breast, ovarian, and cervical cancer</title>
            <link>http://www.medworm.com/index.php?rid=3369765&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F4t2977k2t7267280%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Tumor neovascularization is a complex process that plays a crucial role in the development of many different types of cancer.
 Vascular endothelial growth factor (VEGF) is a potent mitogen that is involved with mitogenesis, angiogenesis, endothelial
 survival, and the induction of hematopoiesis. By increasing vascular permeability in endothelial cells, it helps tumors recruit
 wound-healing proteins fibrin and fibrinogen from the plasma, suggesting that tumor formation is a process of abnormal wound
 healing dependent on the ability to generate a blood supply. The human female reproductive tract is highly dependent on VEGF
 for normal functions such as endometrial proliferation and development of the corpus luteum. The unique influence of female
 sex steroid hormones on...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3369765</comments>
            <pubDate>Sun, 14 Mar 2010 12:26:49 +0100</pubDate>
            <guid isPermaLink="false">3369765</guid>        </item>
        <item>
            <title>VHL and PTEN loss coordinate to promote mouse liver vascular lesions</title>
            <link>http://www.medworm.com/index.php?rid=3362077&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F3qw4314488701m74%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Von Hippel-Lindau (VHL) inactivation develops a tumor syndrome characterized by highly vascularized tumors as a result of hypoxia inducible factors
 (HIF) stabilization. The most common manifestation is the development of hemangioblastomas typically located in the central
 nervous system and other organs including the liver. PTEN (Phosphatase and tension homologue deleted on chromosome 10) inactivation also upregulates HIF-1α and may take part in promoting
 vascular lesions in tumors. The coordinate effect of loss of these tumor suppressors on HIF levels, and the subsequent effect
 on vascular lesion formation would elucidate the potential for mechanisms to modify HIF dosage supplementally and impact tumor
 phenotype. We therefore employed models of somatic conditional...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3362077</comments>
            <pubDate>Thu, 11 Mar 2010 02:45:21 +0100</pubDate>
            <guid isPermaLink="false">3362077</guid>        </item>
        <item>
            <title>Transcriptional regulation of the vascular endothelial glycome by angiogenic and inflammatory signalling</title>
            <link>http://www.medworm.com/index.php?rid=3287231&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb12425g72521524p%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Vascular endothelial cells undergo many molecular changes during pathological processes such as inflammation and tumour development.
 Tumours such as malignant lymphomas affecting bone marrow are dependent on interactions with endothelial cells for (1) site-specific
 homing and (2) tumour-induced angiogenesis. Modifications in glycosylation are responsible for fine-tuning of distinct endothelial
 surface receptors. In order to gain a comprehensive insight into the regulation of the endothelial glycome, comprising genes
 encoding for sugar transporters (sugar s/t), glycosyltransferases (GT), glycan-degrading enzymes (GD) and lectins (GBP), we
 performed gene profiling analysis of the human bone marrow–derived microvascular endothelial cell line HBMEC-60 that resembles
...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3287231</comments>
            <pubDate>Wed, 17 Feb 2010 06:59:05 +0100</pubDate>
            <guid isPermaLink="false">3287231</guid>        </item>
        <item>
            <title>A switch in Notch gene expression parallels stem cell to endothelial transition in infantile hemangioma</title>
            <link>http://www.medworm.com/index.php?rid=3171306&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fc88351j340j25120%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;HemSCs have distinct Notch expression patterns from differentiated HemECs and from normal human endothelial cells. Notch3
 is expressed in HemSCs, while Notch1, Notch4, and Jagged-1 have higher expression levels in HemECs. Notch3 was localized to
 the interstitial cells outside of the nascent vascular channels in proliferating IH tissue sections, but became more apparent
 in the perivascular cells in involuting IH. In summary, the pattern of Notch gene expression mirrors the progression from
 immature cells to endothelial-lined vascular channels (i.e., endothelial differentiation) that characterizes the growth and
 involution of IH.
 
 
 
	Content Type Journal ArticleCategory Original PaperDOI 10.1007/s10456-009-9161-5Authors
		June K. Wu, Columbia University, College...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3171306</comments>
            <pubDate>Tue, 12 Jan 2010 18:20:49 +0100</pubDate>
            <guid isPermaLink="false">3171306</guid>        </item>
        <item>
            <title>Anti-angiogenic tyrosine kinase inhibitors: what is their mechanism of action?</title>
            <link>http://www.medworm.com/index.php?rid=3088735&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fe75714u240323749%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Tyrosine kinases are important cellular signaling proteins that have a variety of biological activities including cell proliferation
 and migration. Multiple kinases are involved in angiogenesis, including receptor tyrosine kinases such as the vascular endothelial
 growth factor receptor. Inhibition of angiogenic tyrosine kinases has been developed as a systemic treatment strategy for
 cancer. Three anti-angiogenic tyrosine kinase inhibitors (TKIs), sunitinib, sorafenib and pazopanib, with differential binding
 capacities to angiogenic kinases were recently approved for treatment of patients with advanced cancer (renal cell cancer,
 gastro-intestinal stromal tumors, and hepatocellular cancer). Many other anti-angiogenic TKIs are being studied in phase I-III
 clinical tr...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3088735</comments>
            <pubDate>Fri, 11 Dec 2009 06:53:53 +0100</pubDate>
            <guid isPermaLink="false">3088735</guid>        </item>
        <item>
            <title>Pigment epithelium–derived factor down regulates hyperglycemia-induced apoptosis via PI3K/Akt activation in goat retinal pericytes</title>
            <link>http://www.medworm.com/index.php?rid=2988478&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft230706g24vt3493%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Pigment epithelium–derived factor (PEDF) is a well-known protease inhibitor for angiogenesis in the eye, suggesting that loss
 of PEDF in eye is implicated in the pathogenesis of proliferative diabetic retinopathy. Since the role of PEDF in diabetic
 retinopathy is unclear, the effect of PEDF on different types of cells constituting the blood vessel has to be checked. Here,
 we have investigated the effects of PEDF under hyperglycemic conditions in retinal pericytes, isolated from goat’s eye and
 used to analyze the signaling pathway involved. High glucose increased the apoptotic cell death and intracellular reactive
 oxygen species generation, which was blocked on the addition of PEDF. PEDF was found to inhibit the apoptotic cell death and
 protect the cells via ac...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2988478</comments>
            <pubDate>Wed, 11 Nov 2009 07:18:31 +0100</pubDate>
            <guid isPermaLink="false">2988478</guid>        </item>
        <item>
            <title>Anti-angiogenic actions of pyrrolidine dithiocarbamate, a nuclear factor kappa B inhibitor</title>
            <link>http://www.medworm.com/index.php?rid=2954000&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Faq7245rj36430672%2F</link>
            <description>In this study, we tested the anti-angiogenic properties
 of pyrrolidine dithiocarbamate (PDTC), a NF-κB inhibitor, using established in vitro and ex vivo assays in human umbilical
 vein endothelial cells (HUVEC) and human metastatic RCC cell lines (ACHN and SN12K1). In vitro, PDTC inhibited proliferation,
 capillary tube formation, invasion and trans-differentiation of HUVEC. Ex vivo, PDTC blocked vessel sprouting from aortic
 explants and disrupted the integrity of pre-formed vessels. PDTC also inhibited the adhesion of HUVEC and RCC cells to substratum
 and inhibited their invasion. PDTC inhibited RCC-induced proliferation of HUVEC. Protein microarray demonstrated heterogenic
 actions in each cell line: in HUVEC, epidermal growth factor was significantly decreased; in ACHN, basic fibrob...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2954000</comments>
            <pubDate>Fri, 30 Oct 2009 18:32:00 +0100</pubDate>
            <guid isPermaLink="false">2954000</guid>        </item>
        <item>
            <title>Capillary arterialization requires the bone marrow-derived cell (BMC)-specific expression of chemokine (C-C motif) receptor-2, but BMCs do not transdifferentiate into microvascular smooth muscle</title>
            <link>http://www.medworm.com/index.php?rid=2836053&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft425005286131382%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Chemokine (C-C motif) receptor-2 (CCR2) regulates arteriogenesis and angiogenesis, facilitating the MCP-1-dependent recruitment
 of growth factor-secreting bone marrow-derived cells (BMCs). Here, we tested the hypothesis that the BMC-specific expression
 of CCR2 is also required for new arteriole formation via capillary arterialization. Following non-ischemic saphenous artery
 occlusion, we measured the following in gracilis muscles: monocyte chemotactic protein-1 (MCP-1) in wild-type (WT) C57Bl/6J
 mice by ELISA, and capillary arterialization in WT–WT and CCR2−/−–WT (donor–host) bone marrow chimeric mice, as well as BMC transdifferentiation in EGFP+–WT mice, by smooth muscle (SM) α-actin immunochemistry. MCP-1 levels were significantly elevated 1&amp;nbsp;day ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2836053</comments>
            <pubDate>Thu, 24 Sep 2009 05:53:44 +0100</pubDate>
            <guid isPermaLink="false">2836053</guid>        </item>
        <item>
            <title>NDRG1 and CRK-I/II are regulators of endothelial cell migration under intermittent hypoxia</title>
            <link>http://www.medworm.com/index.php?rid=2812148&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F17042830560x0un2%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Intermittent Hypoxia (IH) that develops in neovascularized solid tumours has been described to positively influence the tumour
 growth by modulating the behaviour of cancer cells as well as of endothelial cells. However, the molecular mechanisms regulated
 by IH still remain poorly understood. In this work, the effects of IH were investigated on endothelial cells by a proteomic
 approach. Protein abundance variations were studied using fluorescent 2D-Differential in Gel Electrophoresis (2D-DIGE). Amongst
 the proteins of which the abundance varied under IH, NDRG1 and CRK-I/II were identified by mass spectrometry. These proteins
 have already been described to influence cancer cell migration as well as the angiogenic processes in solid tumours. Since
 an increase in endo...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2812148</comments>
            <pubDate>Thu, 17 Sep 2009 12:32:08 +0100</pubDate>
            <guid isPermaLink="false">2812148</guid>        </item>
        <item>
            <title>Computer-aided quantification of retinal neovascularization</title>
            <link>http://www.medworm.com/index.php?rid=2812149&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy61t41w9v6457436%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Rodent models of retinal angiogenesis play a pivotal role in angiogenesis research. These models are a window to developmental
 angiogenesis, to pathological retinopathy, and are also in&amp;nbsp;vivo tools for anti-angiogenic drug screening in cancer and ophthalmic
 research. The mouse model of oxygen-induced retinopathy (OIR) has emerged as one of the leading in&amp;nbsp;vivo models for these purposes.
 Many of the animal studies that laid the foundation for the recent breakthrough of anti-angiogenic treatments into clinical
 practice were performed in the OIR model. However, readouts from the OIR model have been time-consuming and can vary depending
 on user experience. Here, we present a computer-aided quantification method that is characterized by (i) significantly improve...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2812149</comments>
            <pubDate>Wed, 16 Sep 2009 13:08:57 +0100</pubDate>
            <guid isPermaLink="false">2812149</guid>        </item>
        <item>
            <title>Nanoparticle-mediated targeting of phosphatidylinositol-3-kinase signaling inhibits angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=2708457&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fq328344378m7t333%2F</link>
            <description>Conclusion&amp;nbsp;&amp;nbsp;Our study, for the first time, shows that targeting of the PI3K pathway using nanoparticles can offer an attractive strategy
 for inhibiting tumor angiogenesis.
 
 
 
	Content Type Journal ArticleDOI 10.1007/s10456-009-9154-4Authors
		Rania Harfouche, Brigham and Women’s Hospital, Harvard Medical School Harvard-MIT Division of Health Sciences and Technology Boston MA 02115 USASudipta Basu, Brigham and Women’s Hospital, Harvard Medical School Harvard-MIT Division of Health Sciences and Technology Boston MA 02115 USAShivani Soni, Brigham and Women’s Hospital, Harvard Medical School Harvard-MIT Division of Health Sciences and Technology Boston MA 02115 USADirk M. Hentschel, Brigham and Women’s Hospital, Harvard Medical School Department of Medicine Boston MA 0211...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2708457</comments>
            <pubDate>Fri, 14 Aug 2009 16:54:33 +0100</pubDate>
            <guid isPermaLink="false">2708457</guid>        </item>
        <item>
            <title>PEDF inhibits VEGF- and EPO- induced angiogenesis in retinal endothelial cells through interruption of PI3K/Akt phosphorylation</title>
            <link>http://www.medworm.com/index.php?rid=2681416&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk920553u72606238%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Retinal angiogenesis in diabetes may lead to visual impairment and even irreversible blindness in people of working age group
 worldwide. The main pathological feature of proliferative diabetic retinopathy (PDR) is hypoxia, and overproduction of growth
 factors like vascular endothelial growth factor (VEGF) and erythropoietin (Epo). This results in pathological proliferation
 of retinal endothelial cells (RECs), leading to new vessel formation (angiogenesis). Inhibition of angiogenesis is a promising
 strategy for treatment of PDR and other retinal neovascular disorders. Pigment epithelium-derived factor (PEDF), a 50-kDa
 protein secreted by retinal pigment epithelium, inhibits the growth of new blood vessel induced in the eye in a variety of
 ways with a yet elusive me...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2681416</comments>
            <pubDate>Thu, 06 Aug 2009 08:21:45 +0100</pubDate>
            <guid isPermaLink="false">2681416</guid>        </item>
        <item>
            <title>Influence of the oxygen microenvironment on the proangiogenic potential of human endothelial colony forming cells</title>
            <link>http://www.medworm.com/index.php?rid=2504195&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fbq294607p3455221%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Therapeutic angiogenesis is a promising strategy to promote the formation of new or collateral vessels for tissue regeneration
 and repair. Since changes in tissue oxygen concentrations are known to stimulate numerous cell functions, these studies have
 focused on the oxygen microenvironment and its role on the angiogenic potential of endothelial cells. We analyzed the proangiogenic
 potential of human endothelial colony-forming cells (hECFCs), a highly proliferative population of circulating endothelial
 progenitor cells, and compared outcomes to human dermal microvascular cells (HMVECs) under oxygen tensions ranging from 1%
 to 21% O2, representative of ischemic or healthy tissues and standard culture conditions. Compared to HMVECs, hECFCs (1) exhibited
 significantly...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2504195</comments>
            <pubDate>Mon, 22 Jun 2009 06:38:23 +0100</pubDate>
            <guid isPermaLink="false">2504195</guid>        </item>
        <item>
            <title>A highly selective, orally bioavailable, vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor has potent activity in vitro and in vivo</title>
            <link>http://www.medworm.com/index.php?rid=2504196&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj513lj6h2550wg71%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Angiogenesis is a complex process that relies on a variety of growth factors and signaling pathways to stimulate endothelial
 cell responses and establish functional blood vessels. Signaling through the vascular endothelial growth factor (VEGF) receptors
 is an important mediator of angiogenesis, a hallmark of tumor growth and metastasis. Inhibition of signaling through VEGF
 has been clinically validated with FDA-approvals of bevacizumab, sorafenib, and suntinib. Our goal was to discover an orally
 available, selective VEGFR-2 inhibitor. A novel oxime, 1-{4-[6-amino-5-(methoxyimino-methyl)-pyrimidin-4-yloxy]-2-chloro-phenyl}-3-ethyl-urea
 (JNJ-38158471), was identified as a potent and selective inhibitor of VEGFR-2. While JNJ-38158471 shares some structure features
 wi...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2504196</comments>
            <pubDate>Mon, 22 Jun 2009 06:38:21 +0100</pubDate>
            <guid isPermaLink="false">2504196</guid>        </item>
        <item>
            <title>Semaphorins and tumor angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=2439869&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fwj4282u523117211%2F</link>
            <description>Content Type Journal ArticleCategory ErratumDOI 10.1007/s10456-009-9149-1Authors
		Guido Serini, Institute for Cancer Research and Treatment 10060 Torino Candiolo ItalyFederica Maione, Institute for Cancer Research and Treatment 10060 Torino Candiolo ItalyEnrico Giraudo, Institute for Cancer Research and Treatment 10060 Torino Candiolo ItalyFederico Bussolino, Institute for Cancer Research and Treatment 10060 Torino Candiolo Italy
	

	
		Journal AngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2439869</comments>
            <pubDate>Wed, 27 May 2009 06:16:08 +0100</pubDate>
            <guid isPermaLink="false">2439869</guid>        </item>
        <item>
            <title>Single and combined effects of αvβ3- and α5β1-integrins on capillary tube formation in a human fibrinous matrix</title>
            <link>http://www.medworm.com/index.php?rid=2422787&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw0u608217817u225%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The fibrinous exudate of a wound or tumor stroma facilitates angiogenesis. We studied the involvement of RGD-binding integrins
 during tube formation in human plasma-derived fibrin clots and human purified fibrin matrices. Capillary-like tube formation
 by human microvascular endothelial cells in a 3D plasma-derived fibrinous matrix was induced by FGF-2 and TNF-α and depended
 largely on cell-bound u-PA and plasmin activities. While tube formation was minimally affected by the addition of either the
 αvβ3-integrin inhibiting mAb LM609 or the α5-integrin inhibiting mAb IIA1, the general RGD-antagonist echistatin completely
 inhibited this process. Remarkably, when αvβ3- and α5β1-integrins were inhibited simultaneously, tube formation was reduced
 by 78%. It was a...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2422787</comments>
            <pubDate>Sat, 16 May 2009 05:59:23 +0100</pubDate>
            <guid isPermaLink="false">2422787</guid>        </item>
        <item>
            <title>The role of the Angiopoietins in vascular morphogenesis</title>
            <link>http://www.medworm.com/index.php?rid=2422786&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F66767lt232287588%2F</link>
            <description>Abstracts&amp;nbsp;&amp;nbsp;The Angiopoietin/Tie system acts as a vascular specific ligand/receptor system to control endothelial cell survival and vascular
 maturation. The Angiopoietin family includes four ligands (Angiopoietin-1, Angiopoietin-2 and Angiopoietin-3/4) and two corresponding
 tyrosine kinase receptors (Tie1 and Tie2). Ang-1 and Ang-2 are specific ligands of Tie2 binding the receptor with similar
 affinity. Tie2 activation promotes vessel assembly and maturation by mediating survival signals for endothelial cells and
 regulating the recruitment of mural cells. Ang-1 acts in a paracrine agonistic manner inducing Tie2 phosphorylation and subsequent
 vessel stabilization. In contrast, Ang-2 is produced by endothelial cells and acts as an autocrine antagonist of Ang-1-mediated
 Tie2 ac...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2422786</comments>
            <pubDate>Sat, 16 May 2009 05:59:23 +0100</pubDate>
            <guid isPermaLink="false">2422786</guid>        </item>
        <item>
            <title>Wnt2 acts as an angiogenic growth factor for non-sinusoidal endothelial cells and inhibits expression of stanniocalcin-1</title>
            <link>http://www.medworm.com/index.php?rid=2422788&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ful720150m88445q7%2F</link>
            <description>In conclusion, we provide evidence that Wnt2 acts as an angiogenic factor for non-sinusoidal
 endothelium in vitro and in vivo whose target genes undergo complex regulation by the tissue microenvironment.
 
	Content Type Journal ArticleCategory Original paperDOI 10.1007/s10456-009-9145-5Authors
		Diana Klein, University Medical Center Mannheim, Ruprecht-Karl University Heidelberg Department of Dermatology, Venereology and Allergology Theodor-Kutzer-Ufer 1-3 68167 Mannheim GermanyAlexandra Demory, University Medical Center Mannheim, Ruprecht-Karl University Heidelberg Department of Dermatology, Venereology and Allergology Theodor-Kutzer-Ufer 1-3 68167 Mannheim GermanyFrancis Peyre, University Medical Center Mannheim, Ruprecht-Karl University Heidelberg Department of Dermatology, Venereology...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2422788</comments>
            <pubDate>Fri, 15 May 2009 06:13:10 +0100</pubDate>
            <guid isPermaLink="false">2422788</guid>        </item>
        <item>
            <title>Vasculogenesis in infantile hemangioma</title>
            <link>http://www.medworm.com/index.php?rid=2413373&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fnt753l0722607p7h%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Infantile hemangioma is a vascular tumor that occurs in 5–10% of infants of European descent. A defining feature of infantile
 hemangioma is the dramatic growth and development into a disorganized mass of blood vessels. Subsequently, a slow spontaneous
 involution begins around 1&amp;nbsp;year of age and continues for 4–6&amp;nbsp;years. The growth and involution of infantile hemangioma is very
 different from other vascular tumors and vascular malformations, which do not regress and can occur at any time during childhood
 or adult life. Much has been learned from careful study of the tissue morphology and gene expression patterns during the life-cycle
 of hemangioma. Tissue explants and tumor-derived cell populations have provided further insight to unravel the cellular an...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2413373</comments>
            <pubDate>Sun, 10 May 2009 05:46:44 +0100</pubDate>
            <guid isPermaLink="false">2413373</guid>        </item>
        <item>
            <title>The endothelial cell tube formation assay on basement membrane turns 20: state of the science and the art</title>
            <link>http://www.medworm.com/index.php?rid=2386555&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F513mq8v754287618%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;It has been more than 20&amp;nbsp;years since it was first demonstrated that endothelial cells will rapidly form capillary-like structures
 in vitro when plated on top of a reconstituted basement membrane extracellular matrix (BME, Matrigel, EHS matrix, etc.). Subsequently,
 this morphological differentiation has been demonstrated with a variety of endothelial cells; with endothelial progenitor
 cells; and with transformed/immortalized endothelial cells. The differentiation process involves several steps in blood vessel
 formation, including cell adhesion, migration, alignment, protease secretion, and tubule formation. Because the formation
 of vessel structures is rapid and quantifiable, endothelial cell differentiation on basement membrane has found numerous applications
...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2386555</comments>
            <pubDate>Tue, 28 Apr 2009 13:37:33 +0100</pubDate>
            <guid isPermaLink="false">2386555</guid>        </item>
        <item>
            <title>Analysis of PPARα-dependent and PPARα-independent transcript regulation following fenofibrate treatment of human endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=2340211&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj7478700r74057q7%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Fenofibrate is a synthetic ligand for the nuclear receptor peroxisome proliferator-activated receptor (PPAR) alpha and has
 been widely used in the treatment of metabolic disorders, especially hyperlipemia, due to its lipid-lowering effect. The molecular
 mechanism of lipid-lowering is relatively well defined: an activated PPARα forms a PPAR–RXR heterodimer and this regulates
 the transcription of genes involved in energy metabolism by binding to PPAR response elements in their promoter regions, so-called
 “trans-activation”. In addition, fenofibrate also has anti-inflammatory and anti-athrogenic effects in vascular endothelial
 and smooth muscle cells. We have limited information about the anti-inflammatory mechanism of fenofibrate; however, “trans-repression...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2340211</comments>
            <pubDate>Thu, 09 Apr 2009 06:49:38 +0100</pubDate>
            <guid isPermaLink="false">2340211</guid>        </item>
        <item>
            <title>Shear stress-induced transcriptional regulation via hybrid promoters as a potential tool for promoting angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=2295664&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy2143075l961222n%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Among the key effects of fluid shear stress on vascular endothelial cells is modulation of gene expression. Promoter sequences
 termed shear stress response elements (SSREs) mediate the responsiveness of endothelial genes to shear stress. While previous
 studies showed that shear stress responsiveness is mediated by a single SSRE, these endogenous promoters often encode for
 multiple SSREs. Moreover, hybrid promoters encoding a single SSRE rarely respond to shear stress at the same magnitude as
 the endogenous promoter. Thus, to better understand the interplay between the various SSREs, and between SSREs and endothelial-specific
 sequences (ESS), we generated a series of constructs regulated by SSREs cassettes alone, or in combination with ESS, and tested
 their respons...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2295664</comments>
            <pubDate>Thu, 26 Mar 2009 08:29:45 +0100</pubDate>
            <guid isPermaLink="false">2295664</guid>        </item>
        <item>
            <title>Sendai viral vector mediated angiopoietin-1 gene transfer for experimental ischemic limb disease</title>
            <link>http://www.medworm.com/index.php?rid=2295667&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx1082003157673p4%2F</link>
            <description>In this study, we constructed a human Ang-1-expressing Sendai viral
 vector (SeVhAng-1) and injected it into the ischemic limb of rats. We found that SeVhAng-1 improved the blood flow recovery
 and increased the capillary density of the ischemic limb, compared with the controls. We also found that SeVhAng-1 increased
 p-Akt during the early period of limb ischemia, and decreased apoptosis in ischemic limb. It suggests that SeVhAng-1 may serve
 as a potential therapeutic tool in ischemic limb disease.
 
	Content Type Journal ArticleCategory Original PaperDOI 10.1007/s10456-009-9144-6Authors
		Jianhua Huang, Sapporo Medical University Department of Molecular Medicine South 1, West 17, Chuo-ku Sapporo 060-8556 JapanMakoto Inoue, DNAVEC Research Corporation Tsukuba, Ibaraki JapanMamoru Hasegaw...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2295667</comments>
            <pubDate>Thu, 26 Mar 2009 08:29:43 +0100</pubDate>
            <guid isPermaLink="false">2295667</guid>        </item>
        <item>
            <title>Cooperation between integrin ανβ3 and VEGFR2 in angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=2258301&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv5nw351u42548312%2F</link>
            <description>This article discusses several possible mechanisms reported
 by different labs which mediate formation of the complex between VEGFR-2 and αvβ3 on endothelial cells. The pathological consequences and regulatory events involved in this receptor cross-talk are also presented.
 
	Content Type Journal ArticleCategory Review PaperDOI 10.1007/s10456-009-9141-9Authors
		Payaningal R. Somanath, The Cleveland Clinic Joseph J. Jacobs Center for Thrombosis and Vascular Biology, Department of Molecular Cardiology, NB50, Lerner Research Institute 9500 Euclid Avenue Cleveland OH 44195 USANikolay L. Malinin, The Cleveland Clinic Joseph J. Jacobs Center for Thrombosis and Vascular Biology, Department of Molecular Cardiology, NB50, Lerner Research Institute 9500 Euclid Avenue Cleveland OH 44195 USATatiana...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2258301</comments>
            <pubDate>Sun, 08 Mar 2009 09:55:23 +0100</pubDate>
            <guid isPermaLink="false">2258301</guid>        </item>
        <item>
            <title>Semaphorins and tumor angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=2249050&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fqg718822141qv334%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Semaphorins belong to a large family of proteins well-conserved along evolution from viruses to mammalians. Secreted and membrane-bound
 semaphorins participate in a wide range of biological phenomena including development and regeneration of nervous system,
 cardiovascular development, and immune system activities. Different classes of semaphorins are bifunctional and often exert
 opposite effects (i.e., repellent or attractive) by acting through the plexin receptor family. However, some classes use other
 membrane receptors and the same plexin-mediated signals may be modulated by co-receptors, in particular neuropilins or some
 tyrosine kinase receptors. In cancer, semaphorins have both tumor-suppressor and tumor-promoting functions, by acting on both
 tumor and strom...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2249050</comments>
            <pubDate>Fri, 06 Mar 2009 11:59:41 +0100</pubDate>
            <guid isPermaLink="false">2249050</guid>        </item>
        <item>
            <title>Chloride intracellular channel 4 is involved in endothelial proliferation and morphogenesis in vitro</title>
            <link>http://www.medworm.com/index.php?rid=2227092&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fd726h2p31x7446uu%2F</link>
            <description>We report the effects of inhibiting or inducing CLIC4 expression on distinct aspects of endothelial
 cell behavior in vitro. Our experiments utilized RNA interference to establish cultured human endothelial cell lines with
 significant reduction of CLIC4 expression, and a CLIC4-expressing lentiviral plasmid was used to establish CLIC4 overexpression
 in endothelial cells. We observed no effect on cell migration and a modest effect on cell survival. Reduced CLIC4 expression
 decreased cell proliferation, capillary network formation, capillary-like sprouting, and lumen formation. This suggests that
 normal endogenous CLIC4 expression is required for angiogenesis and tubulogenesis. Accordingly, increased CLIC4 expression
 promoted proliferation, network formation, capillary-like sprouting, an...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2227092</comments>
            <pubDate>Fri, 27 Feb 2009 10:45:48 +0100</pubDate>
            <guid isPermaLink="false">2227092</guid>        </item>
        <item>
            <title>Cell surface nucleolin antagonist causes endothelial cell apoptosis and normalization of tumor vasculature</title>
            <link>http://www.medworm.com/index.php?rid=2204925&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F5442l6k7385l012l%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Nucleolin is specifically transported to the surface of proliferating endothelial cells in vitro and in vivo. In contrast
 to its well defined functions in the nucleus and cytoplasm, the function of cell surface nucleolin is poorly defined. We have
 previously identified the nucleolin-binding antibody NCL3 that specifically binds to cell surface nucleolin on angiogenic
 blood vessels in vivo and is internalized into the cell. Here, we show that NCL3 inhibits endothelial tube formation in vitro
 as well as angiogenesis in the matrigel plaque assay and subcutaneous tumor models in vivo. Intriguingly, the specific targeting
 of proliferating endothelial cells by NCL3 in subcutaneous tumor models leads to the normalization of the tumor vasculature
 and as a result to an inc...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2204925</comments>
            <pubDate>Thu, 19 Feb 2009 14:23:40 +0100</pubDate>
            <guid isPermaLink="false">2204925</guid>        </item>
        <item>
            <title>Role of endothelial progenitors and other bone marrow-derived cells in the development of the tumor vasculature</title>
            <link>http://www.medworm.com/index.php?rid=2200336&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm702j81958567662%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Increasing evidence suggests the importance of bone marrow-derived cells for blood vessel formation (neovascularization) in
 tumors, which can occur in two mechanisms: angiogenesis and vasculogenesis. Angiogenesis results from proliferation and sprouting
 of existing blood vessels close to the tumor, while vasculogenesis is believed to arise from recruitment of circulating cells,
 largely derived from the bone marrow, and de novo clonal formation of blood vessels from these cells. Although bone marrow-derived
 cells are crucial for neovascularization, current evidence suggests a promotional role of these cells on the existing blood
 vessels rather than de novo neovascularization in tumors. This is believed to be due to the highly proangiogenic features
 of these cells. ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2200336</comments>
            <pubDate>Tue, 17 Feb 2009 13:01:50 +0100</pubDate>
            <guid isPermaLink="false">2200336</guid>        </item>
        <item>
            <title>Fibronectins in vascular morphogenesis</title>
            <link>http://www.medworm.com/index.php?rid=2190451&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk704v1j1788u2600%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Fibronectin is an extracellular matrix protein found only in vertebrate organisms containing endothelium-lined vasculature
 and is required for cardiovascular development in fish and mice. Fibronectin and its splice variants containing EIIIA and
 EIIIB domains are highly upregulated around newly developing vasculature during embryogenesis and in pathological conditions
 including atherosclerosis, cardiac hypertrophy, and tumorigenesis. However, their molecular roles in these processes are not
 entirely understood. We review genetic studies examining functions of fibronectin and its splice variants during embryonic
 cardiovascular development, and discuss potential roles of fibronectin in vascular disease and tumor angiogenesis.
 
	Content Type Journal ArticleCategory Re...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2190451</comments>
            <pubDate>Sat, 14 Feb 2009 07:58:29 +0100</pubDate>
            <guid isPermaLink="false">2190451</guid>        </item>
        <item>
            <title>A comparative study on the anti-angiogenic effects of DNA-damaging and cytoskeletal-disrupting agents</title>
            <link>http://www.medworm.com/index.php?rid=2187639&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv2091mm1x6615380%2F</link>
            <description>We report that bleomycin, mitomycin C and
 cytoskeletal-disrupting drugs (2-methoxyestradiol, taxol, vincristine, vinblastine, colchicine, nocodazole, and cytochalasin
 D) exhibit anti-angiogenic activities of varying potency. Bleomycin and the various cytoskeletal-disrupting drugs inhibited
 endothelial cell migration, while mitomycin C had a marginal effect. Both DNA-damaging and cytoskeletal-disrupting drugs decreased
 endothelial cell growth in a dose-dependent manner, and this was accompanied by the induction of apoptosis. The growth inhibitory
 and apoptotic effects of cytoskeletal-disrupting drugs were the most pronounced. We also show that both classes of drugs inhibited
 capillary-like tube formation in an assay of in vitro angiogenesis, with cytoskeletal-disrupting agents inhibit...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2187639</comments>
            <pubDate>Fri, 13 Feb 2009 08:29:06 +0100</pubDate>
            <guid isPermaLink="false">2187639</guid>        </item>
        <item>
            <title>Increased numbers of small circulating endothelial cells in renal cell cancer patients treated with sunitinib</title>
            <link>http://www.medworm.com/index.php?rid=2187640&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F675l2723r6154006%2F</link>
            <description>In conclusion, opposite kinetics
 of two circulating CD34bright cell populations, HPCs and small CECs, were observed in sunitinib-treated RCC patients. The increase in CECs is likely caused
 by sunitinib targeting of immature tumor vessels.
 
	Content Type Journal ArticleCategory Original PaperDOI 10.1007/s10456-009-9133-9Authors
		Laura Vroling, VU University Medical Center Department of Medical Oncology CCA 2-54, De Boelelaan 1117 1081 HV Amsterdam The NetherlandsAstrid A. M. van der Veldt, VU University Medical Center Department of Medical Oncology CCA 2-54, De Boelelaan 1117 1081 HV Amsterdam The NetherlandsRichard R. de Haas, VU University Medical Center Department of Medical Oncology CCA 2-54, De Boelelaan 1117 1081 HV Amsterdam The NetherlandsJohn B. A. G. Haanen, The Netherlands Ca...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2187640</comments>
            <pubDate>Thu, 12 Feb 2009 07:24:30 +0100</pubDate>
            <guid isPermaLink="false">2187640</guid>        </item>
        <item>
            <title>Molecular differentiation and specialization of vascular beds</title>
            <link>http://www.medworm.com/index.php?rid=2187641&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fdu2853200h124h27%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Transport in the large and complex bodies of vertebrate organisms is mediated by extensive and highly branched tubular networks
 that are formed by endothelial cells. Blood vessels are responsible for systemic circulation, while the lymphatic vasculature
 drains extravasated plasma, proteins, particles, and cells from the interstitium. Endothelial cells of blood vessels and lymphatic
 vessels can be distinguished by the expression of certain molecular markers, which accompany or even contribute to functional
 and morphological differences. Even within the blood vessel network, some molecules and pathways selectively mark the endothelium
 of arteries, veins and capillaries and are thought to contribute to the differentiation of these vessels. Moreover, microvessels
 can ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2187641</comments>
            <pubDate>Thu, 12 Feb 2009 07:24:28 +0100</pubDate>
            <guid isPermaLink="false">2187641</guid>        </item>
        <item>
            <title>Intussusceptive angiogenesis and its role in vascular morphogenesis, patterning, and remodeling</title>
            <link>http://www.medworm.com/index.php?rid=2167455&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fd4814g17200h61hv%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;New blood vessels arise initially as blood islands in the process known as vasculogenesis or as new capillary segments produced
 through angiogenesis. Angiogenesis itself encompasses two broad processes, namely sprouting (SA) and intussusceptive (IA)
 angiogenesis. Primordial capillary plexuses expand through both SA and IA, but subsequent growth and remodeling are achieved
 through IA. The latter process proceeds through transluminal tissue pillar formation and subsequent vascular splitting, and
 the direction taken by the pillars delineates IA into overt phases, namely: intussusceptive microvascular growth, intussusceptive
 arborization, and intussusceptive branching remodeling. Intussusceptive microvascular growth circumscribes the process of
 initiation of pillar fo...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2167455</comments>
            <pubDate>Thu, 05 Feb 2009 07:07:23 +0100</pubDate>
            <guid isPermaLink="false">2167455</guid>        </item>
        <item>
            <title>Intermittent hypoxia is an angiogenic inducer for endothelial cells: role of HIF-1</title>
            <link>http://www.medworm.com/index.php?rid=2147491&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F3122081816744413%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The presence of hypoxia in tumor and its role in promoting angiogenesis are well-established. Recently, in addition to chronic
 hypoxia, cycling or intermittent hypoxia has also been demonstrated. However, its role in inducing new blood vessel formation
 is less clear. This work is aimed to investigate whether intermittent hypoxia can induce a pro-angiogenic phenotype in endothelial
 cells, in vitro. We studied changes in the expression of genes involved in inflammation and angiogenesis under intermittent
 and chronic hypoxia. We evidenced genes specifically expressed under intermittent hypoxia, suggesting different cell responses
 induced by intermittent versus chronic hypoxia. An increase in the expression of pro-angiogenic and pro-inflammatory genes
 under intermitte...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2147491</comments>
            <pubDate>Thu, 29 Jan 2009 11:09:47 +0100</pubDate>
            <guid isPermaLink="false">2147491</guid>        </item>
        <item>
            <title>Endogenous endothelial cell signaling systems maintain vascular stability</title>
            <link>http://www.medworm.com/index.php?rid=2141268&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft86k8318227wx0pp%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The function of the endothelium is to provide a network to allow delivery of oxygen and nutrients to tissues throughout the
 body. This network comprises adjacent endothelial cells that utilize adherens junction proteins such as vascular endothelial
 cadherin (VE-cadherin) to maintain the appropriate level of vascular permeability. The disruption of VE-cadherin interactions
 during pathologic settings can lead to excessive vascular leak with adverse effects. Endogenous cell signaling systems have
 been defined, which help to maintain the proper level of vascular stability. Perhaps the best described system is Angiopoietin-1
 (Ang-1). Ang-1 acting through its receptor Tie2 generates a well-described set of signaling events ultimately leading to enhanced
 vascular stabili...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2141268</comments>
            <pubDate>Tue, 27 Jan 2009 07:55:03 +0100</pubDate>
            <guid isPermaLink="false">2141268</guid>        </item>
        <item>
            <title>Morphological and molecular aspects of physiological vascular morphogenesis</title>
            <link>http://www.medworm.com/index.php?rid=2094699&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F9451452810082t8v%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The cardiovascular system plays a crucial role in vertebrate development and homeostasis. Several genetic and epigenetic mechanisms
 are involved in the early development of the vascular system. During embryonal life, blood vessels first appear as the result
 of vasculogenesis, whereas remodeling of the primary vascular plexus occurs by angiogenesis. Many tissue-derived factors are
 involved in blood vessel formation and evidence is emerging that endothelial cells themselves represent a source of instructive
 signals to non-vascular tissue cells during organ development. This review article summarizes our knowledge concerning the
 principal factors involved in the regulation of vascular morphogenesis.
 
	Content Type Journal ArticleCategory Original PaperDOI 10.1007/s10...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2094699</comments>
            <pubDate>Thu, 08 Jan 2009 09:04:38 +0100</pubDate>
            <guid isPermaLink="false">2094699</guid>        </item>
        <item>
            <title>Tyrosine phosphatase beta regulates angiopoietin-Tie2 signaling in human endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=2073736&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fqw041617144706t3%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;These results reveal a novel role for HPTPβ in modulating Ang-1-Tie2 signaling and endothelial cell survival.
 
 
 
	Content Type Journal ArticleCategory Original PaperDOI 10.1007/s10456-008-9126-0Authors
		Orisha K. Yacyshyn, St Michael’s Hospital Terrence Donnelly Heart Centre and Division of Cardiology 30 Bond St. Toronto ON M5B 1W8 CanadaPatrick F. H. Lai, St Michael’s Hospital Terrence Donnelly Heart Centre and Division of Cardiology 30 Bond St. Toronto ON M5B 1W8 CanadaKelly Forse, University of Toronto Human Biology Program Toronto ON M5S 1A8 CanadaKrystyna Teichert-Kuliszewska, St Michael’s Hospital Terrence Donnelly Heart Centre and Division of Cardiology 30 Bond St. Toronto ON M5B 1W8 CanadaPaul Jurasz, St Michael’s Hospital Terrence Donnelly Heart...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2073736</comments>
            <pubDate>Wed, 31 Dec 2008 10:00:43 +0100</pubDate>
            <guid isPermaLink="false">2073736</guid>        </item>
        <item>
            <title>Osteoprotegerin and RANKL differentially regulate angiogenesis and endothelial cell function</title>
            <link>http://www.medworm.com/index.php?rid=2065168&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F6367m64033502553%2F</link>
            <description>In this study, we assessed the role of OPG and its ligands, receptor activator
 of nuclear factor-κB ligand (RANKL) and tumor necrosis factor-related apoptosis inducing ligand (TRAIL), in microvessel formation
 using the rat aortic ring model of angiogenesis. OPG was found to promote a twofold increase in angiogenic sprouting in the
 aortic ring model, and this effect was inhibited by pre-incubation with a fivefold molar excess of either RANKL or TRAIL.
 While TRAIL had no effect upon angiogenesis on its own, RANKL was found to potently inhibit basal and vascular endothelial
 growth factor-induced angiogenesis. OPG increased the rate of endothelial cell proliferation in sprouting microvessels; in
 contrast, RANKL inhibited proliferation. RANKL was found to induce endothelial apoptosis at ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2065168</comments>
            <pubDate>Tue, 23 Dec 2008 07:15:55 +0100</pubDate>
            <guid isPermaLink="false">2065168</guid>        </item>
        <item>
            <title>Gα13 regulates MEF2-dependent gene transcription in endothelial cells: role in angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=2052526&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F9t61505m02126v51%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The α subunit of heterotrimeric G13 protein is required for the embryonic angiogenesis (Offermanns et al., Science 275:533–536,
 1997). However, the molecular mechanism of Gα13-dependent angiogenesis is not understood. Here, we show that myocyte-specific
 enhancer factor-2 (MEF2) mediates Gα13-dependent angiogenesis. Our data showed that constitutively activated Gα13Q226L stimulated
 MEF2-dependent gene transcription. In addition, downregulation of endogenous Gα13 inhibited thrombin-stimulated MEF2-dependent
 gene transcription in endothelial cells. Both Ca2+/calmodulin-dependent kinase IV (CaMKIV) and histone deacetylase 5 (HDAC5) were involved in Gα13-mediated MEF2-dependent gene
 transcription. Gα13Q226L also increased Ca2+/calmodulin-independent CaMKIV acti...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2052526</comments>
            <pubDate>Thu, 18 Dec 2008 07:03:46 +0100</pubDate>
            <guid isPermaLink="false">2052526</guid>        </item>
        <item>
            <title>Molecular imaging of tumor angiogenesis using αvβ3-integrin targeted multimodal quantum dots</title>
            <link>http://www.medworm.com/index.php?rid=2032962&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F2n5745074877u611%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Molecular imaging of angiogenesis is urgently needed for diagnostic purposes such as early detection, monitoring of (angiostatic)
 therapy and individualized therapy. Multimodality molecular imaging is a promising and refined technique to study tumor angiogenesis,
 which has so far been largely unexplored due to the lack of suitable multimodal contrast agents. Here, we report on the application
 of a novel αvβ3-specific quantum dot-based nanoparticle, which has been optimized for both optical and magnetic resonance
 detection of tumor angiogenesis. Upon intravenous injection of RGD-pQDs in tumor-bearing mice, intravital microscopy allowed
 the detection of angiogenically activated endothelium at cellular resolution with a small scanning window and limited penetration
...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2032962</comments>
            <pubDate>Wed, 10 Dec 2008 08:04:05 +0100</pubDate>
            <guid isPermaLink="false">2032962</guid>        </item>
        <item>
            <title>A nuclease-resistant RNA aptamer specifically inhibits angiopoietin-1-mediated Tie2 activation and function</title>
            <link>http://www.medworm.com/index.php?rid=1996165&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy3x646277266466l%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Tie2 is a receptor tyrosine kinase that is expressed predominantly in the endothelium and plays key roles in both physiological
 and pathological angiogenesis. The ligands for Tie2, the angiopoietins (Ang), perform opposing functions in vascular maintenance
 and angiogenesis; Ang1 regulates vascular quiescence, while Ang2 is thought to promote vascular destabilization and facilitate
 angiogenesis. However, the mechanisms responsible for these differences are not understood. To begin to elucidate the molecular
 differences between the angiopoietins, we previously developed a specific RNA aptamer inhibitor of Ang2. Here, we used the
 same iterative in&amp;nbsp;vitro selection process, termed SELEX (Systematic Evolution of Ligands by EXponential enrichment), to screen a librar...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1996165</comments>
            <pubDate>Thu, 27 Nov 2008 09:47:10 +0100</pubDate>
            <guid isPermaLink="false">1996165</guid>        </item>
        <item>
            <title>Anti-tumoral effect of active immunotherapy in C57BL/6 mice using a recombinant human VEGF protein as antigen and three chemically unrelated adjuvants</title>
            <link>http://www.medworm.com/index.php?rid=1996166&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff25511052g180204%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Following the clinical success of Bevacizumab, a humanized monoclonal antibody that affects the interaction between vascular
 endothelial growth factor (VEGF) and its receptors, blocking tumor-induced angiogenesis has become one of the most important
 targets for the development of new cancer therapeutic drugs and procedures. Among the latter, therapeutic vaccination using
 VEGF as antigen presents itself as very attractive, with the potential of generating not only a growth factor blocking antibody
 response but also a cellular response against tumor cells and stromal elements, which appear to be a major source of tumor
 VEGF. In this paper, we report the development of a protein vaccine candidate, based on a human modified VEGF antigen that
 is expressed at high level...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1996166</comments>
            <pubDate>Wed, 26 Nov 2008 19:52:23 +0100</pubDate>
            <guid isPermaLink="false">1996166</guid>        </item>
        <item>
            <title>Angiogenic response to extracorporeal shock wave treatment in murine skin isografts</title>
            <link>http://www.medworm.com/index.php?rid=1946982&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft6245j7850q0r2m6%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Skin grafts are commonly utilized and proven effective methods of open wound coverage. Revascularization through neoangiogenesis
 is a pivotal mechanism for skin graft integration and durability. Extracorporeal shock-wave treatment (ESWT) has been demonstrated
 to accelerate wound repair; however, its mechanism-of-action is unclear. We investigated the role of ESWT in early revascularization
 of full-thickness skin isografts in a murine model. Cohorts of mice were euthanized and skin grafts were harvested 6&amp;nbsp;h, 2,
 4, and 7&amp;nbsp;days post grafting&amp;nbsp;±&amp;nbsp;ESWT. Various aspects of graft neovascularization were measured including gross morphology,
 quantitative microscopy (vessel number, density), immunohistochemistry (CD31), cDNA SuperArrays for 84 angiogenesis-...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1946982</comments>
            <pubDate>Sun, 09 Nov 2008 10:05:22 +0100</pubDate>
            <guid isPermaLink="false">1946982</guid>        </item>
        <item>
            <title>Circulating and imaging markers for angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=1888051&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F8111753830j41383%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Abundant preclinical and indirect clinical data have for several decades convincingly supported the notion that anti-angiogenesis
 is an effective strategy for the inhibition of tumor growth. The recent success achieved in patients with metastatic colon
 carcinoma using a neutralizing antibody directed against vascular endothelial growth factor (VEGF) has translated preclinical
 optimism into a clinical reality.With this transformation in the field of angiogenesis has come a need for reliable surrogate
 markers. A surrogate marker by definition serves as a substitute for the underlying process in question, and in the case of
 angiogenesis, microvessel density (usually in so-called “hot-spots”) has until now been the most widely used parameter. However,
 this paramet...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1888051</comments>
            <pubDate>Fri, 17 Oct 2008 09:49:22 +0100</pubDate>
            <guid isPermaLink="false">1888051</guid>        </item>
        <item>
            <title>PPARγ ligands, rosiglitazone and pioglitazone, inhibit bFGF- and VEGF-mediated angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=1825371&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg88mk73g02q64081%2F</link>
            <description>Conclusions&amp;nbsp;&amp;nbsp;These results suggest that PPARγ ligands, pioglitazone and rosiglitazone, in addition to their important regulatory role in
 adipogenesis and inflammation, possess anti-angiogenic properties. Thus, PPARγ ligands may be useful in the treatment of diabetic
 retinopathy, macular degeneration, and other ocular disorders and may lower the risk to develop cancer in diabetic patients.
 
 
 
	Content Type Journal ArticleCategory Original PaperDOI 10.1007/s10456-008-9118-0Authors
		Ahmad Aljada, Long Island University, C.W. Post. Department of Biomedical Sciences Brookville NY USALaura O’Connor, The Pharmaceutical Research Institute (PRI), Albany College of Pharmacy Albany NY USAYu-Yen Fu, Long Island University, C.W. Post. Department of Biomedical Sciences Brookville NY ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1825371</comments>
            <pubDate>Tue, 23 Sep 2008 10:06:57 +0100</pubDate>
            <guid isPermaLink="false">1825371</guid>        </item>
        <item>
            <title>A role for planar cell polarity signaling in angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=1806135&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F61t534742m331500%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The planar cell polarity (PCP) pathway is a highly conserved signaling cascade that coordinates both epithelial and axonal
 morphogenic movements during development. Angiogenesis also involves the growth and migration of polarized cells, although
 the mechanisms underlying their intercellular communication are poorly understood. Here, using cell culture assays, we demonstrate
 that inhibition of PCP signaling disrupts endothelial cell growth, polarity, and migration, all of which can be rescued through
 downstream activation of this pathway by expression of either Daam-1, Diversin or Inversin. Silencing of either Dvl2 or Prickle
 suppressed endothelial cell proliferation. Moreover, loss of p53 rescues endothelial cell growth arrest but not the migration
 inhibition caus...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1806135</comments>
            <pubDate>Wed, 17 Sep 2008 08:33:12 +0100</pubDate>
            <guid isPermaLink="false">1806135</guid>        </item>
        <item>
            <title>The chick embryo chorioallantoic membrane as a model to study tumor metastasis</title>
            <link>http://www.medworm.com/index.php?rid=1782516&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fd5534w557130x29x%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Tumor metastasis represents a major problem in the treatment of patients with different cancers. Specific phenotype and behavior
 of metastatic cells derive from specific molecular mechanisms involved in consecutive steps of the metastatic process. Several
 in&amp;nbsp;vitro and in&amp;nbsp;vivo experimental models have been utilized, but they cannot completely reproduce and characterize each step
 of the metastatic process. This review article is focused on the chick embryo chorioallantoic membrane as an in&amp;nbsp;vivo model
 to study the metastatic process.
 
	Content Type Journal ArticleCategory Review PaperDOI 10.1007/s10456-008-9117-1Authors
		Anca Maria Cimpean, “Victor Babes” University of Medicine and Pharmacy Timisoara Department of Histology Timisoara RomaniaDomenic...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1782516</comments>
            <pubDate>Tue, 09 Sep 2008 11:17:24 +0100</pubDate>
            <guid isPermaLink="false">1782516</guid>        </item>
        <item>
            <title>Farnesyltransferase inhibitors target multiple endothelial cell functions in angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=1749980&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy544t24p2816qmn2%2F</link>
            <description>We examined the effects of FTI treatment on a range of assays designed to pick apart the individual functions
 of endothelial cells during angiogenesis. We found that FTIs inhibit endothelial cell proliferation, causing a failure of
 mitosis and accumulation of binucleate cells. FTIs also block the directional migration of endothelial cells toward VEGF,
 the major pro-angiogenic factor in adult tissues. In a co-culture assay of angiogenesis, FTI treatment significantly inhibits
 tube formation, but has no effect on pre-existing structures. Defects in tube formation could be replicated by specific targeting
 of endothelial cell farnesyltransferase using RNA interference. Our data show that FTIs directly target endothelial cells
 in angiogenesis, explaining previous in&amp;nbsp;vivo findings. Im...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1749980</comments>
            <pubDate>Sat, 30 Aug 2008 10:22:59 +0100</pubDate>
            <guid isPermaLink="false">1749980</guid>        </item>
        <item>
            <title>The discovery of the placental growth factor and its role in angiogenesis: a historical review</title>
            <link>http://www.medworm.com/index.php?rid=1537803&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fd515336763l87708%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The placental growth factor (PlGF) is an angiogenic protein belonging to the vascular endothelial growth factor (VEGF) family,
 which was discovered in 1991 by an Italian scientist, Maria Graziella Persico. Dr Persico cloned and purified PlGF and determined
 its structure by crystallography resolution. Furthermore, she identified VEGF receptor-1 (VEGFR-1) as the receptor for PlGF,
 and in collaboration with Dr Peter Carmeliet in Leuven, she generated evidence that loss of PlGF does not affect development,
 reproduction, or postnatal life. PlGF is expressed primarily in the placenta and is up-regulated in several pathological conditions,
 although its role is still controversial. Some data in literature reported that PlGF enhances pathological angiogenesis by
 initiating...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1537803</comments>
            <pubDate>Sat, 21 Jun 2008 07:06:53 +0100</pubDate>
            <guid isPermaLink="false">1537803</guid>        </item>
        <item>
            <title>Lysophosphatidic acid (LPA) and angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=1475057&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F11j5177662767176%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Lysophosphatidic acid (LPA) is a simple lipid with many important biological functions such as the regulation of cellular
 proliferation, cellular migration, differentiation, and suppression of apoptosis. Although a direct angiogenic effect of LPA
 has not been reported to date, there are indications that LPA promotes angiogenesis. In addition, LPA is a chemoattractant
 for cultured endothelial cells and promotes barrier function in such cultures [1]. To test the hypothesis that LPA is angiogenic, we used the chicken chorio-allantoic membrane (CAM) assay. Sequence analysis
 of the cloned, full-length chicken LPA receptor cDNAs revealed three receptor types that are orthologous to the mammalian
 LPA1, LPA2, and LPA3 receptors. We document herein that LPA is angiogenic in...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1475057</comments>
            <pubDate>Tue, 27 May 2008 05:52:45 +0100</pubDate>
            <guid isPermaLink="false">1475057</guid>        </item>
        <item>
            <title>Angiogenic-regulatory network revealed by molecular profiling heart tissue following Akt1 induction in endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=1463642&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw3338h4101026803%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Akt is a pivotal signaling molecule involved in the regulation of angiogenesis. In order to further elucidate the role of
 Akt1 in blood vessel development, a tetracycline-regulated transgenic system was utilized to conditionally activate Akt1 signaling
 in endothelial cells to examine transcript expression changes associated with angiogenesis in the heart. Induction of Akt1
 over the course of 6&amp;nbsp;weeks led to a 33% increase in capillary density without affecting overall heart growth. Transcript expression
 profiles in the hearts were analyzed with an Affymetrix GeneChip Mouse Expression Set 430 2.0, which represents approximately
 45,000 cDNAs and ESTs. A total of 248 transcripts were differentially expressed between transgenic and control mice (fold
 change&amp;nbsp;&amp;...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1463642</comments>
            <pubDate>Tue, 20 May 2008 06:00:04 +0100</pubDate>
            <guid isPermaLink="false">1463642</guid>        </item>
        <item>
            <title>Akt1 is necessary for the vascular maturation and angiogenesis during cutaneous wound healing</title>
            <link>http://www.medworm.com/index.php?rid=1380474&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F754611072274711t%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Previous in&amp;nbsp;vivo and in&amp;nbsp;vitro studies have shown that Akt1 serves as a crucial regulator of vascular maturation, extracellular
 matrix composition, and angiogenesis in tumors. Hence, we hypothesized that Akt1 may be necessary for other angiogenesis-dependent
 processes, including wound healing. Using Akt1
 −/− and Akt2
 −/− mice, we demonstrate that deficiency of Akt1, but not Akt2, results in impaired assembly of collagen in skin wounds and around
 the blood vessels. Wounds in Akt1
 −/− mice, but not in Akt2
 −/− mice, were characterized by reduced vascular area as well as impaired vascular maturation as evidenced by reduced smooth
 muscle cell recruitment. Expression level of a major angiogenic growth factor, VEGF, was significantly lower in ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1380474</comments>
            <pubDate>Wed, 16 Apr 2008 14:55:13 +0100</pubDate>
            <guid isPermaLink="false">1380474</guid>        </item>
        <item>
            <title>Novel function of the thyroid hormone analog tetraiodothyroacetic acid: a cancer chemosensitizing and anti-cancer agent</title>
            <link>http://www.medworm.com/index.php?rid=1351917&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fm2l008740n6u124l%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Previous studies from our laboratory have demonstrated that thyroid hormones play a key role in cancer progression. In addition,
 a deaminated form, tetraiodothyroacetic acid (tetrac), that antagonizes the proliferative action of these hormones was found
 to possess anti-cancer functions through its ability to inhibit cellular proliferation and angiogenesis. The present study
 was undertaken to investigate whether tetrac could also suppress the development of drug resistance, known as a causative
 factor of disease relapse. Tetrac was shown to enhance cellular response in vitro to doxorubicin, etoposide, cisplatin, and
 trichostatin A in resistant tumor cell lines derived from neuroblastoma, osteosarcoma, and breast cancer. The mechanism of
 action of tetrac did not inv...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1351917</comments>
            <pubDate>Thu, 03 Apr 2008 08:16:23 +0100</pubDate>
            <guid isPermaLink="false">1351917</guid>        </item>
        <item>
            <title>VEGF165 expression in the tumor microenvironment influences the differentiation of bone marrow-derived pericytes that contribute to the Ewing’s sarcoma vasculature</title>
            <link>http://www.medworm.com/index.php?rid=1310918&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fu7603176423130h0%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;We previously demonstrated that bone marrow (BM) cells migrate to Ewing’s tumors and differentiate into endothelial cells
 within the tumor vasculature. Recent evidence suggests that the roles of BM cells in tumors are more diverse. We investigated
 whether non-endothelial cell types critical for tumor vessel development are also derived from migrated BM cells. We utilized
 BM transplantation with GFP+ transgenic mice as BM donors and nude mice as recipients to track the fate of migrated BM cells. After engraftment, we injected
 recipient mice either subcutaneously or intramuscularly with Ewing’s sarcoma cells. We labeled functional tumor vessels using
 intravascular perfusion staining with tomato lectin. We assessed BM cell recruitment/differentiation within the tu...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1310918</comments>
            <pubDate>Sun, 16 Mar 2008 05:43:45 +0100</pubDate>
            <guid isPermaLink="false">1310918</guid>        </item>
        <item>
            <title>Anti-angiogenic activity of sesterterpenes; natural product inhibitors of FGF-2-induced angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=1300223&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fv41v55k7175282qg%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Angiogenesis, the growth of new blood vessels from the pre-existing vasculature is of physiological and pathological importance.
 We have investigated the anti-angiogenic potential of two naturally occurring sesterterpenes, leucosesterterpenone (compound
 1) and leucosterlactone (compound 2) isolated from the Himalayan plant Leucosceptrum canum and identified as having biological activity in preliminary screening. Compound 1 inhibited fibroblast growth factor-2-induced proliferation, migration in a wounding assay, chemotaxis and tube formation
 with small vessel (human dermal) and large vessel (bovine aortic) endothelial cells while compound 2 was largely inactive. Both compounds were also active in an in&amp;nbsp;vivo angiogenic model using the chick chorioallantoic membra...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1300223</comments>
            <pubDate>Tue, 11 Mar 2008 08:29:26 +0100</pubDate>
            <guid isPermaLink="false">1300223</guid>        </item>
        <item>
            <title>Mechanisms of adaptive angiogenesis to tissue hypoxia</title>
            <link>http://www.medworm.com/index.php?rid=1294251&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp817440xv0722022%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Angiogenesis is mostly an adaptive response to tissue hypoxia, which occurs under a wide variety of situations ranging from
 embryonic development to tumor growth. In general, angiogenesis is dependent on the accumulation of hypoxia inducible factors
 (HIFs), which are heterodimeric transcription factors of α and β subunits. Under normoxia, HIF heterodimers are not abundantly
 present due to oxygen dependent hydroxylation, polyubiquitination, and proteasomal degradation of α subunits. Under hypoxia,
 however, α subunits are stabilized and form heterodimers with HIF-1β which is not subject to oxygen dependent regulation.
 The accumulation of HIFs under hypoxia allows them to activate the expression of many angiogenic genes and therefore initiates
 the angiogenic pro...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1294251</comments>
            <pubDate>Mon, 10 Mar 2008 05:33:21 +0100</pubDate>
            <guid isPermaLink="false">1294251</guid>        </item>
        <item>
            <title>Video monitoring of neovessel occlusion induced by photodynamic therapy with verteporfin (Visudyne®), in the CAM model</title>
            <link>http://www.medworm.com/index.php?rid=1290935&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk9301027022w2487%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The aim of the present study was to monitor photodynamic angioocclusion with verteporfin in capillaries. Details of this process
 were recorded under a microscope in real-time using a high-sensitivity video camera. A procedure was developed based on intravenous
 (i.v.) injection of a light-activated drug, Visudyne®, into the chorioallantoic membrane (CAM) of a 12-day-old chicken embryo. The effect of light activation was probed after
 24&amp;nbsp;h by i.v. injection of a fluorescent dye (FITC dextran), and analysis of its fluorescence distribution. The angioocclusive
 effect was graded based on the size of the occluded vessels, and these results were compared with clinical observations. The
 time-resolved thrombus formation taking place in a fraction of the field of view w...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1290935</comments>
            <pubDate>Fri, 07 Mar 2008 06:56:59 +0100</pubDate>
            <guid isPermaLink="false">1290935</guid>        </item>
        <item>
            <title>In memoriam Dr. Judah Folkman</title>
            <link>http://www.medworm.com/index.php?rid=1282176&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ff5l298m230072627%2F</link>
            <description>Content Type Journal ArticleCategory ObituaryDOI 10.1007/s10456-008-9103-7Authors
		Joyce Bischoff, Karp Family Research Laboratories Vascular Biology Program, Children’s Hospital Boston 300 Longwood Ave. Boston MA 02115 USAArjan W. Griffioen, University Hospital Maastricht Department of Pathology 6202 AZ Maastricht The Netherlands
	

	
		Journal AngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1282176</comments>
            <pubDate>Tue, 04 Mar 2008 08:31:59 +0100</pubDate>
            <guid isPermaLink="false">1282176</guid>        </item>
        <item>
            <title>Hedgehog signalling in vascular development</title>
            <link>http://www.medworm.com/index.php?rid=1265076&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ffq168r8408267215%2F</link>
            <description>This article reviews the role of Hedgehog signalling in both
 embryonic and postnatal vascular development. The temporal importance of a window of hedgehog dependent angiogenesis during
 development is emphasised and illustrated using a whole mouse embryo culture system.
 
	Content Type Journal ArticleCategory Original PaperDOI 10.1007/s10456-008-9105-5Authors
		Takashi Nagase, National Hospital Organisation Murayama Medical Centre Clinical Research Centre Musashimurayam-shi Tokyo 208–0011 JapanMiki Nagase, University of Tokyo Graduate School of Medicine Department of Nephrology and Endocrinology 7-3-1 Hongo Bunkyo-ku, Tokyo 113-8655 JapanMasafumi Machida, National Hospital Organisation Murayama Medical Centre Clinical Research Centre Musashimurayam-shi Tokyo 208–0011 JapanToshiro Fuji...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1265076</comments>
            <pubDate>Wed, 27 Feb 2008 15:56:11 +0100</pubDate>
            <guid isPermaLink="false">1265076</guid>        </item>
        <item>
            <title>Vascular permeability, vascular hyperpermeability and angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=1258045&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fpur514283w75up8r%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The vascular system has the critical function of supplying tissues with nutrients and clearing waste products. To accomplish
 these goals, the vasculature must be sufficiently permeable to allow the free, bidirectional passage of small molecules and
 gases and, to a lesser extent, of plasma proteins. Physiologists and many vascular biologists differ as to the definition
 of vascular permeability and the proper methodology for its measurement. We review these conflicting views, finding that both
 provide useful but complementary information. Vascular permeability by any measure is dramatically increased in acute and
 chronic inflammation, cancer, and wound healing. This hyperpermeability is mediated by acute or chronic exposure to vascular
 permeabilizing agents, particu...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1258045</comments>
            <pubDate>Fri, 22 Feb 2008 15:47:39 +0100</pubDate>
            <guid isPermaLink="false">1258045</guid>        </item>
        <item>
            <title>Endoglin in angiogenesis and vascular diseases</title>
            <link>http://www.medworm.com/index.php?rid=1246556&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj64298670681r017%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Endoglin is a transmembrane auxillary receptor for transforming growth factor-β (TGF-β) that is predominantly expressed on
 proliferating endothelial cells. Endoglin deficient mice die during midgestation due to cardiovascular defects. Mutations
 in endoglin and activin receptor-like kinase 1 (ALK1), an endothelial specific TGF-β type I receptor, have been linked to
 hereditary hemorrhagic telangiectasia (HHT), an autosomal dominant vascular dysplasia characterized by telangiectases and
 arteriovenous malformations. Endoglin heterozygote mice develop HHT-like vascular abnormalities, have impaired tumor and post-ischemic
 angiogenesis and demonstrate an endothelial nitric oxide synthase-dependent deterioration in the regulation of vascular tone.
 In pre-eclampsia, pla...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1246556</comments>
            <pubDate>Tue, 19 Feb 2008 15:45:08 +0100</pubDate>
            <guid isPermaLink="false">1246556</guid>        </item>
        <item>
            <title>Neuropilin structure governs VEGF and semaphorin binding and regulates angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=1246555&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fb16g218546265107%2F</link>
            <description>This article reviews the latest information of NRP structure and
 how structure influences angiogenesis. In addition, the role of NRPs in human cancer is addressed.
 
	Content Type Journal ArticleCategory Original PaperDOI 10.1007/s10456-008-9097-1Authors
		Elena Geretti, Children’s Hospital and Harvard Medical School Department of Surgery, Vascular Biology Program Karp Building 12210, 300 Longwood Ave. Boston MA 02115 USAAkio Shimizu, Children’s Hospital and Harvard Medical School Department of Surgery, Vascular Biology Program Karp Building 12210, 300 Longwood Ave. Boston MA 02115 USAMichael Klagsbrun, Children’s Hospital and Harvard Medical School Department of Surgery, Vascular Biology Program Karp Building 12210, 300 Longwood Ave. Boston MA 02115 USA
	

	
		Journal AngiogenesisO...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1246555</comments>
            <pubDate>Tue, 19 Feb 2008 15:45:08 +0100</pubDate>
            <guid isPermaLink="false">1246555</guid>        </item>
        <item>
            <title>NF-κB: a new player in angiostatic therapy</title>
            <link>http://www.medworm.com/index.php?rid=1246554&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F317007063822n441%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Angiogenesis is considered a promising target in the treatment of cancer. Most of the angiogenesis inhibitors in late-stage
 clinical testing or approved for the treatment of cancer act indirectly on endothelial cells. They either neutralize angiogenic
 growth factors from the circulation or block the signaling pathways activated by these growth factors. Another group of angiogenesis
 inhibitors are the direct angiostatic compounds. These agents have a direct effect on the endothelium, affecting cellular
 regulatory pathways, independently of the tumor cells. The reason that this category of agents is lagging behind regarding
 their translation to the clinic may be the lack of sufficient knowledge on the mechanism of action of these compounds. The
 transcription factor ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1246554</comments>
            <pubDate>Tue, 19 Feb 2008 15:45:08 +0100</pubDate>
            <guid isPermaLink="false">1246554</guid>        </item>
        <item>
            <title>From the editor</title>
            <link>http://www.medworm.com/index.php?rid=1236871&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk167632ju50266p7%2F</link>
            <description>Content Type Journal ArticleCategory Editorial notesDOI 10.1007/s10456-008-9104-6Authors
		Roy Bicknell, Institute of Biomedical Research, University of Birmingham Centre for Cardiovascular Sciences Wolfson Drive Edgbaston Birmingham B15 2TT UKJudy R. van Beijnum, Research Institute for Growth and Development (GROW) Maastricht University Hospital Angiogenesis Laboratory, Department of Pathology PO Box 5800 6202AZ Maastricht The Netherlands
	

	
		Journal AngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1236871</comments>
            <pubDate>Fri, 15 Feb 2008 18:05:59 +0100</pubDate>
            <guid isPermaLink="false">1236871</guid>        </item>
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