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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>Sun, 21 Mar 2010 17:04:01 +0100</lastBuildDate>
        <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>
        <item>
            <title>Fibroblasts potentiate blood vessel formation partially through secreted factor TIMP-1</title>
            <link>http://www.medworm.com/index.php?rid=1234540&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fx7v460v476505m24%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;During wound repair, new blood vessels form in response to angiogenic signals emanating from injured tissues. Dermal fibroblasts
 are known to play an important role in wound healing, and have been linked to angiogenesis; therefore, we sought to understand
 the mechanisms through which these cells control blood vessel formation. Using a three-dimensional angiogenesis assay we demonstrate
 that dermal fibroblasts enhance the tube-forming potential of endothelial cells, and this augmentation is partially due to
 secreted factors present in conditioned media. Interestingly, we identified tissue inhibitor of metalloproteinase-1 (TIMP-1)
 as a factor uniquely secreted by fibroblasts, and addition of exogenous TIMP-1 increased vessel assembly. The enhancing activity
 of TIMP-...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1234540</comments>
            <pubDate>Thu, 14 Feb 2008 16:07:22 +0100</pubDate>
            <guid isPermaLink="false">1234540</guid>        </item>
        <item>
            <title>Developmental Vascular Biology Workshop III</title>
            <link>http://www.medworm.com/index.php?rid=1229156&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F90028n7755555275%2F</link>
            <description>Content Type Journal ArticleCategory AbstractDOI 10.1007/s10456-008-9090-8

	
		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=1229156</comments>
            <pubDate>Tue, 12 Feb 2008 17:38:01 +0100</pubDate>
            <guid isPermaLink="false">1229156</guid>        </item>
        <item>
            <title>Netrins and UNC5 receptors in angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=1229155&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh9h7176821875626%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Both neuronal and vascular development require guidance to establish a precise branching pattern of these systems in the vertebrate
 body. Several molecules implicated in axon navigation have also been shown to regulate vessel sprouting. Among these guidance
 cues, Netrins constitute a family of diffusible molecules with a bifuncional role in axon pathfinding. Recent findings implicate
 Netrins in other developmental processes, including vascular development. We here review recent studies and discuss the possible
 dual function of Netrins and its receptors during branching of blood vessels in developmental and pathological angiogenesis.
 
	Content Type Journal ArticleCategory Original PaperDOI 10.1007/s10456-008-9096-2Authors
		Catarina Freitas, Inserm, U833 75005 Paris...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1229155</comments>
            <pubDate>Tue, 12 Feb 2008 17:38:01 +0100</pubDate>
            <guid isPermaLink="false">1229155</guid>        </item>
        <item>
            <title>Convergence and amplification of toll-like receptor (TLR) and receptor for advanced glycation end products (RAGE) signaling pathways via high mobility group B1 (HMGB1)</title>
            <link>http://www.medworm.com/index.php?rid=1225138&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F011366223066w495%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Sustained proinflammatory responses in rheumatoid arthritis, atherosclerosis, and diabetic retinopathy, as well as in cancer,
 are often associated with increased angiogenesis that contributes to tissue disruption and disease progression. High mobility
 group B1 (HMGB1) has been recognized as a proinflammatory cytokine and more recently, as a proangiogenic factor. HMGB1 can
 either be passively released from necrotic cells or actively secreted in response to angiogenic and inflammatory signals.
 HMGB1 itself may signal through the receptor for advanced glycation end products (RAGE), and via toll-like receptors, TLR2
 and TLR4. Activation of these receptors results in the activation of NFκB, which induces the upregulation of leukocyte adhesion
 molecules and the product...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1225138</comments>
            <pubDate>Sun, 10 Feb 2008 03:10:31 +0100</pubDate>
            <guid isPermaLink="false">1225138</guid>        </item>
        <item>
            <title>Slits and Roundabouts in cancer, tumour angiogenesis and endothelial cell migration</title>
            <link>http://www.medworm.com/index.php?rid=1225137&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy00037617971gt16%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Angiogenesis describes the development of new blood vessels from pre-existing vessels. The hijacking of this physiological
 process by tumours allows them to develop their own supplies of nutrients and oxygen, enabling their growth and metastasis.
 A large body of literature has accumulated over the last 20&amp;nbsp;years relating to angiogenesis, including signalling pathways
 involved in this process. One such pathway uses Slit–Roundabout proteins that are implicated in the development of cancers
 and tumour angiogenesis. The Roundabout family of receptors are large, single-pass transmembrane cell surface receptors involved
 in directing cell migration in response to their cognate Slit ligands. Although best known for their role in neuronal development,
 Slits and Round...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1225137</comments>
            <pubDate>Sun, 10 Feb 2008 03:10:31 +0100</pubDate>
            <guid isPermaLink="false">1225137</guid>        </item>
        <item>
            <title>Regulation of angiogenesis by homotypic and heterotypic notch signalling in endothelial cells and pericytes: from basic research to potential therapies</title>
            <link>http://www.medworm.com/index.php?rid=1217837&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fh55086n15642t72g%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The notch-signalling pathway regulates cell fate and differentiation through cell–cell communication. In recent years, several
 in&amp;nbsp;vitro and in&amp;nbsp;vivo studies have demonstrated that notch-signalling functions as a negative feedback mechanism downstream
 of the VEGF-signalling pathway that acts to finely shape the vascular network. Notch activation by the Jagged-1 and Delta-like
 4 ligands regulates different steps of blood vessel development ranging from proliferation and survival of endothelial cells,
 to vessel branching and arterial–venous differentiation. In addition, heterotypic notch signalling from endothelial cells
 to pericytes is critical for vessel stabilization and maturation. Interestingly, several studies have demonstrated that blocking
 the no...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1217837</comments>
            <pubDate>Thu, 07 Feb 2008 18:11:30 +0100</pubDate>
            <guid isPermaLink="false">1217837</guid>        </item>
        <item>
            <title>Letter to the editor</title>
            <link>http://www.medworm.com/index.php?rid=1217836&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr46r52n18530415q%2F</link>
            <description>Content Type Journal ArticleCategory LetterDOI 10.1007/s10456-008-9091-7Authors
		Isaiah Fidler, MD Anderson Cancer Center Department of Cancer Biology 1515 Holcombe Boulevard Houston TX 77030 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=1217836</comments>
            <pubDate>Thu, 07 Feb 2008 18:11:30 +0100</pubDate>
            <guid isPermaLink="false">1217836</guid>        </item>
        <item>
            <title>Wnt/Frizzled signaling in angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=1215180&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F45vv02356r57tg63%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The roles of growth factors such as angiopoietin (Ang) and vascular endothelial growth factor (VEGF) in angiogenesis have
 been known for some time, yet we have just an incipient appreciation for the contribution of Wnts to this process. Cellular
 proliferation and polarity, apoptosis, branching morphogenesis, inductive processes, and the maintenance of stem cells in
 an undifferentiated, proliferative state are all regulated by Wnt signaling. The development and maintenance of vascular structures
 are dependent on all these processes, and their orchestration has, to some extent, been revealed in studies of VEGF and Ang
 receptors. Recent evidence links the Wnt/Frizzled signaling pathway to proper vascular growth in mammals but our knowledge
 of Wnt function in the vasc...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1215180</comments>
            <pubDate>Wed, 06 Feb 2008 15:55:44 +0100</pubDate>
            <guid isPermaLink="false">1215180</guid>        </item>
        <item>
            <title>Judah Folkman, a pioneer in the study of angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=1215181&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft7j20h8115221123%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;More than 30&amp;nbsp;years ago, Judah Folkman found a revolutionary new way to think about cancer. He postulated that in order to
 survive and grow, tumors require blood vessels, and that by cutting off that blood supply, a cancer could be starved into
 remission. What began as a revolutionary approach to cancer has evolved into one of the most exciting areas of scientific
 inquiry today. Over the years, Folkman and a growing team of researchers have isolated the proteins and unraveled the processes
 that regulate angiogenesis. Meanwhile, a new generation of angiogenesis research has emerged as well, widening the field into
 new areas of human disease and deepening it to examine the underlying biological processes responsible for those diseases.
 
	Content Type Journal Art...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1215181</comments>
            <pubDate>Tue, 05 Feb 2008 15:47:40 +0100</pubDate>
            <guid isPermaLink="false">1215181</guid>        </item>
        <item>
            <title>Sprouty proteins, masterminds of receptor tyrosine kinase signaling</title>
            <link>http://www.medworm.com/index.php?rid=1182708&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F6405736144813323%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Angiogenesis relies on endothelial cells properly processing signals from growth factors provided in both an autocrine and
 a paracrine manner. These mitogens bind to their cognate receptor tyrosine kinases (RTKs) on the cell surface, thereby activating
 a myriad of complex intracellular signaling pathways whose outputs include cell growth, migration, and morphogenesis. Understanding
 how these cascades are precisely controlled will provide insight into physiological and pathological angiogenesis. The Sprouty
 (Spry) family of proteins is a highly conserved group of negative feedback loop modulators of growth factor-mediated mitogen-activated
 protein kinase (MAPK) activation originally described in Drosophila. There are four mammalian orthologs (Spry1-4) whose modulati...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1182708</comments>
            <pubDate>Fri, 25 Jan 2008 16:06:35 +0100</pubDate>
            <guid isPermaLink="false">1182708</guid>        </item>
        <item>
            <title>Tetraiodothyroacetic acid, a small molecule integrin ligand, blocks angiogenesis induced by vascular endothelial growth factor and basic fibroblast growth factor</title>
            <link>http://www.medworm.com/index.php?rid=1100025&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F2x183536m57u5j33%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Thyroid hormone has been recently shown to induce tumor growth and angiogenesis via a plasma-membrane hormone receptor on
 integrin αVβ3. The receptor is at or near the Arg-Gly-Asp (RGD) recognition site on the integrin that is important to extracellular
 matrix (ECM) protein and vascular growth factor interactions with the integrin. In the present study, we examined the possibility
 that tetraiodothyroacetic acid (tetrac), a deaminated, non-agonist thyroid hormone analog that binds to the integrin receptor,
 may modulate vascular growth factor-induced angiogenesis in the absence of thyroid hormone. Angiogenesis models were studied
 in which VEGF or FGF2 (1–2&amp;nbsp;μg/ml) induced tube formation in human dermal microvascular endothelial cells (HDMEC), stimulated
 new...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1100025</comments>
            <pubDate>Sat, 15 Dec 2007 20:35:23 +0100</pubDate>
            <guid isPermaLink="false">1100025</guid>        </item>
        <item>
            <title>Extracellular ATP is a pro-angiogenic factor for pulmonary artery vasa vasorum endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=1090369&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg7v88q5644176725%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Expansion of the vasa vasorum network has been observed in a variety of systemic and pulmonary vascular diseases. We recently
 reported that a marked expansion of the vasa vasorum network occurs in the pulmonary artery adventitia of chronically hypoxic
 calves. Since hypoxia has been shown to stimulate ATP release from both vascular resident as well as circulatory blood cells,
 these studies were undertaken to determine if extracellular ATP exerts angiogenic effects on isolated vasa vasorum endothelial
 cells (VVEC) and/or if it augments the effects of other angiogenic factors (VEGF and basic FGF) known to be present in the
 hypoxic microenvironment. We found that extracellular ATP dramatically increases DNA synthesis, migration, and rearrangement
 into tube-like networ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1090369</comments>
            <pubDate>Tue, 11 Dec 2007 15:36:54 +0100</pubDate>
            <guid isPermaLink="false">1090369</guid>        </item>
        <item>
            <title>Differential gene expression analysis of tubule forming and non-tubule forming endothelial cells: CDC42GAP as a counter-regulator in tubule formation</title>
            <link>http://www.medworm.com/index.php?rid=1074858&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr207j86541455m26%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The formation of new tubular structures from a quiescent endothelial lining is one of the hallmarks of sprouting angiogenesis.
 This process can be mimicked in vitro by inducing capillary-like tubular structures in a three-dimensional (3D) fibrin matrix.
 We aimed to analyze the differential mRNA expression in two phenotypically distinct cell populations from the same culture,
 namely in tubule-forming endothelial cells and monolayer endothelial cells not participating in tubule formation. A fibrin-rich
 3D matrix derived from human plasma was used to facilitate tubule formation by human foreskin microvascular endothelial cells
 (hMVEC). After 7&amp;nbsp;days of stimulation with VEGF, bFGF, and TNF-α, the culture consisted of a monolayer and capillary-like sprouts
 that ha...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1074858</comments>
            <pubDate>Mon, 03 Dec 2007 20:10:18 +0100</pubDate>
            <guid isPermaLink="false">1074858</guid>        </item>
        <item>
            <title>RGS5 expression is a quantitative measure of pericyte coverage of blood vessels</title>
            <link>http://www.medworm.com/index.php?rid=1054735&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fy971750123802372%2F</link>
            <description>In this study, we have developed an objective,
 sensitive, and high-throughput method for quantifying pericyte coverage of angiogenic vessels by analyzing the expression
 of the pericyte-specific gene, the regulator of G-protein signaling 5 (RGS5). We determined that RGS5 expression was up-regulated
 during a defined developmental time period in which nascent vessel sprouts acquired a pericyte covering. Furthermore, RGS5
 expression was dramatically reduced in vessels with poor pericyte coverage compared to normal angiogenic vasculature. Finally,
 we determined that the susceptibility of nascent vessels to regression by vascular endothelial growth factor (VEGF) inhibition
 was significantly reduced following RGS5 up-regulation, further implicating RGS5 in pericyte-endothelial cell interact...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1054735</comments>
            <pubDate>Sun, 25 Nov 2007 19:02:39 +0100</pubDate>
            <guid isPermaLink="false">1054735</guid>        </item>
        <item>
            <title>Caveolin-1 polarization in transmigrating endothelial cells requires binding to intermediate filaments</title>
            <link>http://www.medworm.com/index.php?rid=979091&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F613w75789t08w438%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Caveolin-1 influences cell migration through multiple signaling pathways. In a previous report, we have shown that caveolin-1
 is polarized in three-dimensional migrating endothelial cells (EC), and that caveolin-1 accumulation at the front of transmigrating
 cells requires the phosphorylatable Tyr14 residue of caveolin-1. Immuno-electron microscopy further indicated that caveolin-1 was distributed along cytoskeletal structures
 in the anterior of transmigrating EC [Parat MO, Anand-Apte B, Fox PL (Mol Biol Cell 14:3156–3168, 2003)]. In the present study,
 we investigate whether caveolin-1 interacts with intermediate filaments (IF) and whether this interaction is required for
 caveolin-1 polarization in transmigrating cells. The distribution of vimentin is polarized in...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=979091</comments>
            <pubDate>Tue, 23 Oct 2007 14:37:30 +0100</pubDate>
            <guid isPermaLink="false">979091</guid>        </item>
        <item>
            <title>Duffy antigen/receptor for chemokines (DARC) attenuates angiogenesis by causing senescence in endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=979090&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw78164p354php2qx%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Duffy antigen/receptor for chemokines (DARC), expressed on erythrocytes and post-capillary venular endothelial cells, selectively
 binds both CXC and CC chemokines. DARC binds ELR&amp;nbsp;+&amp;nbsp;angiogenic chemokines such as IL-8 (CXCL8). We show that the DARC on endothelial
 cells plays a direct role in regulating angiogenesis. MatrigelTM in&amp;nbsp;vivo plug assay showed that there was more capillary formation in DARC knockout mice compared to wild type mice indicating
 that DARC attenuated angiogenic activity. In&amp;nbsp;vitro angiogenic assay on MatrigelTM coated plates using DARC expressing stable human cerebro-microvascular endothelial cells (HCEC) showed that, although capillary
 formation in transfected cells started early within 4–8&amp;nbsp;h; capillary formation was att...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=979090</comments>
            <pubDate>Tue, 23 Oct 2007 14:37:30 +0100</pubDate>
            <guid isPermaLink="false">979090</guid>        </item>
        <item>
            <title>Anti-angiogenic effects of imatinib target smooth muscle cells but not endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=886172&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fg7026n5856137427%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Knowing that progesterone up-regulates PDGF-A, which plays a relevant role in angiogenesis, and that imatinib mesylate targets
 PDGF receptor tyrosine kinase activity, the aim of the present study was to examine the effects of imatinib on Human Aortic
 Smooth Muscle Cells (HAoSMC) and Human Umbilical Vein Endothelial Cells (HUVEC) after incubation with progesterone. Expression
 of phosphorylated (activated) PDGFR-α was detected in HAoSMC, but in a very low extent in HUVEC. In agreement with the lack
 of active PDGFR-α, imatinib was unable to prevent HUVEC growth, survival or migration ability. In contrast, HAoSMC viability
 and proliferation were effectively inhibited by imatinib, as evaluated by MTT and BrdU incorporation assay, respectively.
 Corroborating these fin...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=886172</comments>
            <pubDate>Tue, 18 Sep 2007 21:07:20 +0100</pubDate>
            <guid isPermaLink="false">886172</guid>        </item>
        <item>
            <title>Angiogenesis as a therapeutic target in arthritis: learning the lessons of the colorectal cancer experience</title>
            <link>http://www.medworm.com/index.php?rid=848255&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fgn37784721k540wh%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The idea of a therapeutic modality aimed at ‘starving’ a tissue of blood vessels, and consequentially of oxygen and nutrients,
 was born from the concept that blood vessel formation (angiogenesis) is central to the progression and maintenance of diseases
 which involve tissue expansion/invasion. In the first instance, solid malignancies were the target for anti-angiogenic treatments,
 with colorectal cancer being the first disease for which an angiogenesis inhibitor—anti-vascular endothelial growth factor
 antibody bevacizumab—was approved in 2004.
 
 Our understanding of the pathogenesis of rheumatoid arthritis (RA) has lead to many parallels being drawn between this chronic
 inflammatory disease and solid tumours, in that both involve tissue expansion, invasio...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=848255</comments>
            <pubDate>Thu, 06 Sep 2007 07:08:35 +0100</pubDate>
            <guid isPermaLink="false">848255</guid>        </item>
        <item>
            <title>Aortic rings stimulate inflammatory angiogenesis in a subcutaneous implant in vivo model</title>
            <link>http://www.medworm.com/index.php?rid=845646&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F2125026287g451h5%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Rat or mouse aortic rings produce angiogenic outgrowths in&amp;nbsp;vitro through endogenous production of growth factors and inflammatory
 cytokines. To further investigate this process in&amp;nbsp;vivo, collagen-Gelfoam constructs containing aortic rings were implanted
 subcutaneously in syngeneic animals. Aortic rings stimulated a prominent angiogenic response characterized by peri- and intra-aortic
 accumulation of florid granulation tissue. Conversely, implants without rings elicited a non-specific inflammatory reaction
 without significant angiogenesis. The angiogenic response to the rings peaked at day 14 and was followed by regression of
 neovessels, which were mostly reabsorbed by day 28. Gene expression studies showed upregulated expression of angiogenic growth
 facto...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=845646</comments>
            <pubDate>Wed, 05 Sep 2007 07:06:53 +0100</pubDate>
            <guid isPermaLink="false">845646</guid>        </item>
        <item>
            <title>Hedgehog signaling in the murine melanoma microenvironment</title>
            <link>http://www.medworm.com/index.php?rid=841583&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F405961765122g8w2%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The Hedgehog intercellular signaling pathway regulates cell proliferation and differentiation. This pathway has been implicated
 to play a role in the pathogenesis of cancer and in embryonic blood vessel development. In the current study, Hedgehog signaling
 in tumor related vasculature and microenvironment was examined using human umbilical vein endothelial cells and B16F0 (murine
 melanoma) tumors models. Use of exogenous Sonic hedgehog (Shh) peptide significantly increased BrdU incorporation in endothelial
 cells in&amp;nbsp;vitro by a factor of 2 (P&amp;nbsp;&amp;lt;&amp;nbsp;0.001). The Hedgehog pathway antagonist cyclopamine effectively reduced Shh-induced proliferation to control levels. To
 study Hedgehog signaling in&amp;nbsp;vivo a hind limb tumor model with the B16F0 cell line w...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=841583</comments>
            <pubDate>Tue, 04 Sep 2007 14:39:29 +0100</pubDate>
            <guid isPermaLink="false">841583</guid>        </item>
        <item>
            <title>Angiogenic response of endothelial cells seeded dispersed versus on beads in fibrin gels</title>
            <link>http://www.medworm.com/index.php?rid=823521&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fn461517323n32426%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Induction of an inter-connected microvessel network in a tissue-engineered construct prior to implantion may be an alternative
 to improve the success rate of cell/tissue survival and wound integration. Conditions of endothelial cell-seeding density
 and distribution were investigated in two 3-D angiogenesis culture systems. Endothelial cells were either seeded dispersed
 in a fibrin gel, or subconfluent on micro-beads (Cytodex�) prior to being embedded in fibrin. Human fibroblasts and growth factors were introduced to optimize angiogenesis. A density
 higher than 4&amp;nbsp;�&amp;nbsp;104 cells/ml of fibrin was necessary to induce angiogenic-like structures (i.e., sprouting, cord-, lumen-like structures) by
 14&amp;nbsp;days in the dispersed cell model. Endothelial cells on mi...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=823521</comments>
            <pubDate>Sun, 26 Aug 2007 08:33:17 +0100</pubDate>
            <guid isPermaLink="false">823521</guid>        </item>
        <item>
            <title>Transcriptome analysis of endothelial cell gene expression induced by growth on matrigel matrices: identification and characterization of MAGP-2 and lumican as novel regulators of angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=778468&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F6085528nkktn6n87%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Remodeling of vascular microenvironments during normal and tumor-induced angiogenesis is an important, yet poorly understood
 mechanism by which endothelial cells (ECs) contribute to the activation or resolution of angiogenesis. We used microarray
 analyses to monitor changes in the transcriptome of ECs undergoing angiogenesis when cultured onto Matrigel matrices. This
 strategy identified 308&amp;nbsp;genes whose expression in ECs was altered at least 3-fold by angiogenesis, of which 63&amp;nbsp;genes were
 found to encode for secretory proteins. In vitro assays that modeled key steps in the angiogenic process showed that several
 identified genes possessed pro- or anti-angiogenic activities (e.g., SMOC-2, secreted modular calcium-binding protein-2; CRELD-2,
 cysteine-rich wit...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778468</comments>
            <pubDate>Sat, 14 Jul 2007 07:09:32 +0100</pubDate>
            <guid isPermaLink="false">778468</guid>        </item>
        <item>
            <title>Thymosin β4 and angiogenesis: modes of action and therapeutic potential</title>
            <link>http://www.medworm.com/index.php?rid=778469&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fwm3w2876167x1451%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Here we review the mechanisms by which Thymosin β4 (Tβ4) regulates angiogenesis, its role in processes, such as wound healing
 and tumour progression and we discuss in more detail the role of Tβ4 in the cardiovascular system and significant recent findings
 implicating Tβ4 as a potential therapeutic agent for ischaemic heart disease.
 
	Content TypeJournal Article

	
		JournalAngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778469</comments>
            <pubDate>Sat, 14 Jul 2007 07:09:31 +0100</pubDate>
            <guid isPermaLink="false">778469</guid>        </item>
        <item>
            <title>Vascular development in embryoid bodies: quantification of transgenic intervention and antiangiogenic treatment</title>
            <link>http://www.medworm.com/index.php?rid=778470&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp31577v211452q36%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;It has become increasingly clear that the investigation of vascular development is best considered in the context of a whole
 tissue environment since in&amp;nbsp;vivo endothelial cells interact closely with other cell types. Murine embryoid bodies have been
 used as a model for the early development of a vascular network and are amenable to genetic manipulation and treatment with
 soluble modulators. However, quantifying morphological changes in these complex three-dimensional structures is challenging.
 In this paper we describe protocols to culture embryoid bodies on a large scale to study vascular development together with
 methods to quantify changes seen when antiangiogenic agents or endothelial cell-specific transgenes are introduced.
 
	Content TypeJournal Article

...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778470</comments>
            <pubDate>Tue, 19 Jun 2007 18:30:59 +0100</pubDate>
            <guid isPermaLink="false">778470</guid>        </item>
        <item>
            <title>T-cadherin suppresses angiogenesis in vivo by inhibiting migration of endothelial cells</title>
            <link>http://www.medworm.com/index.php?rid=778472&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fd26180wk377867p1%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Our previous studies have revealed the abundant expression of T-cadherin—a glycosylphosphatidylinositol (GPI)-anchored member
 of cadherin superfamily—in endothelial and mural cells in the heart and vasculature. The upregulation of T-cadherin in vascular
 proliferative disorders such as atherosclerosis and restenosis suggests the involvement of T-cadherin in vascular growth and
 remodeling. However, the functional significance of this molecule in the vasculature remains unknown. The effect of T-cadherin
 on angiogenesis in&amp;nbsp;vivo was evaluated using Matrigel implant model. We demonstrate that T-cadherin overexpression in L929
 cells injected in Matrigel inhibits neovascularization of the plug. In&amp;nbsp;vitro T-cadherin inhibits the directional migration
 of endoth...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778472</comments>
            <pubDate>Tue, 08 May 2007 12:36:08 +0100</pubDate>
            <guid isPermaLink="false">778472</guid>        </item>
        <item>
            <title>Effect of Src kinase inhibition on metastasis and tumor angiogenesis in human pancreatic cancer</title>
            <link>http://www.medworm.com/index.php?rid=778471&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F5l52xw9q11k36543%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Tumor angiogenesis is a process that requires migration, proliferation, and differentiation of endothelial cells. We hypothesized
 that decrease in pancreatic tumor growth due to inhibition of Src activity is associated with the inability of Src kinase
 to trigger a network of such signaling processes, which finally leads to endothelial cell death and angiogenesis-restricted
 tumor dormancy. The therapeutic efficacy of Src kinase inhibitor AZM475271 was tested in nude mice orthotopically xenografted
 with L3.6pl pancreatic carcinoma cells. No liver metastases and peritoneal carcinosis were detected and a significant effect
 on the average pancreatic tumor burden was observed following treatment with AZM475271, which in turn correlated with a decrease
 in cell proliferat...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778471</comments>
            <pubDate>Tue, 08 May 2007 12:36:05 +0100</pubDate>
            <guid isPermaLink="false">778471</guid>        </item>
        <item>
            <title>Obituary: Graziella Persico</title>
            <link>http://www.medworm.com/index.php?rid=778473&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fk1k47720xx8l5173%2F</link>
            <description>Content TypeJournal Article

	
		JournalAngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778473</comments>
            <pubDate>Fri, 04 May 2007 09:20:53 +0100</pubDate>
            <guid isPermaLink="false">778473</guid>        </item>
        <item>
            <title>Angiogenesis and chronic inflammation: cause or consequence?</title>
            <link>http://www.medworm.com/index.php?rid=778474&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F67796x5u6213p917%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Evidence has been gathered regarding the association between angiogenesis and inflammation in pathological situations. These
 two phenomena have long been coupled together in many chronic inflammatory disorders with distinct etiopathogenic origin,
 including psoriasis, rheumatoid arthritis, Crohn’s disease, diabetes, and cancer. Lately, this concept has further been substantiated
 by the finding that several previously established non-inflammatory disorders, such as osteoarthritis and obesity, display
 both inflammation and angiogenesis in an exacerbated manner. In addition, the interplay between inflammatory cells, endothelial
 cells and fibroblasts in chronic inflammation sites, together with the fact that inflammation and angiogenesis can actually
 be triggered by ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778474</comments>
            <pubDate>Wed, 25 Apr 2007 07:08:49 +0100</pubDate>
            <guid isPermaLink="false">778474</guid>        </item>
        <item>
            <title>Combination therapy for the treatment of ocular neovascularization</title>
            <link>http://www.medworm.com/index.php?rid=778476&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Ft08303h20m087v42%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;The growth of inappropriately regulated, leaky blood vessels is a prominent component of several debilitating eye diseases,
 such as age-related macular degeneration (AMD), proliferative diabetic retinopathy (PDR), and retinopathy of prematurity (ROP).
 New pharmacological therapies that target vascular endothelial growth factor-A (VEGF-A) have significantly enhanced the treatment
 of AMD by limiting the progression of the disease, and in some cases, by improving vision. Although anti-VEGF therapy will
 undoubtedly prove valuable in the treatment of other neovascular diseases of the eye, improvements with this type of therapy
 are still required. At present, anti-VEGF therapy requires intravitreal injection and a relatively frequent dosing regimen
 (4–6&amp;nbsp;weeks). F...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778476</comments>
            <pubDate>Tue, 13 Mar 2007 08:46:38 +0100</pubDate>
            <guid isPermaLink="false">778476</guid>        </item>
        <item>
            <title>Molecular genetics of AMD and current animal models</title>
            <link>http://www.medworm.com/index.php?rid=778478&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fr541165276117906%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;During the past few years systematic investigation into the epidemiology, genetics, and pathophysiology of age-related macular
 degeneration (AMD) has provided important new insight into this leading cause of vision loss in older persons. These studies
 provide a view of AMD as a complex trait influenced by well-established genetic and environmental risks that leads to the
 deposition of inflammatory deposits in the outer retina. This maculopathy leads to visual dysfunction through a variety of
 mechanisms and complications that can be observed in both humans and animal models. In this review, the risks associated with
 AMD in humans and the animal models used to study AMD and its complications will be summarized. No effort has been made to
 perform a comprehensive cita...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778478</comments>
            <pubDate>Tue, 13 Mar 2007 08:46:37 +0100</pubDate>
            <guid isPermaLink="false">778478</guid>        </item>
        <item>
            <title>Ocular drug development - Future Directions</title>
            <link>http://www.medworm.com/index.php?rid=778477&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fj67378342x112430%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Technology has caught up with retinal diseases of neovasculature. Work with anti-cancer, anti-angiogenic agents has fueled
 the way for ocular therapeutics. The market size for age-related macular degeneration and diabetic retinopathy is huge. Fifteen
 million people in the United States alone have age-related macular degeneration with 2 million new cases each year (1). About 20.8 million people in the United States have diabetes. Of those, 14.6 million are diagnosed and 6.2 million are
 undiagnosed (2). Of patients who have had type 1 diabetics for more than 20&amp;nbsp;years, 50% will have proliferative diabetic retinopathy (3). Between 60% and 80% of type 2 diabetics will manifest retinopathy after 15&amp;nbsp;years, and 20% will progress to proliferative
 retinopathy after ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778477</comments>
            <pubDate>Tue, 13 Mar 2007 08:46:37 +0100</pubDate>
            <guid isPermaLink="false">778477</guid>        </item>
        <item>
            <title>Progenitor cells and retinal angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=778475&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F23842244tq408029%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Nothing more dramatically captures the imagination of the visually impaired patient or the ophthalmologist treating them than
 the possibility of rebuilding a damaged retina or vasculature with “stem cells.” Stem cells (SC) have been isolated from adult
 tissues and represent a pool of cells that may serve to facilitate rescue/repair of damaged tissue following injury or stress.
 We propose a new paradigm to “mature” otherwise immature neovasculature or, better yet, stabilize existing vasculature to
 hypoxic damage. This may be possible through the use of autologous bone marrow (BM) or cord blood derived hematopoietic SC
 that selectively target sites of neovascularization and gliosis where they provide vasculo- and neurotrophic effects. We have
 demonstrated th...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778475</comments>
            <pubDate>Tue, 13 Mar 2007 08:46:37 +0100</pubDate>
            <guid isPermaLink="false">778475</guid>        </item>
        <item>
            <title>Vascular permeability in ocular disease and the role of tight junctions</title>
            <link>http://www.medworm.com/index.php?rid=778479&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F8088021137126654%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Vascular permeability is closely linked with angiogenesis in a number of pathologies. In the retina, the normally well-developed
 blood-retinal barrier is altered in a host of eye diseases preceding or commensurate with angiogenesis. This review examines
 the literature regarding the tight junction complex that establishes the blood-retinal barrier focusing on the transmembrane
 proteins occludin and the claudin family and the membrane associated protein zonula occludens. The changes observed in these
 proteins associated with vascular and epithelial permeability is discussed. Finally, novel literature addressing the link
 between the tight junction complex and angiogenesis is considered.
 
	Content TypeJournal Article

	
		JournalAngiogenesisOnline ISSN 1573-7209Print ...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778479</comments>
            <pubDate>Tue, 06 Mar 2007 14:09:53 +0100</pubDate>
            <guid isPermaLink="false">778479</guid>        </item>
        <item>
            <title>Retinopathy of prematurity</title>
            <link>http://www.medworm.com/index.php?rid=778480&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fag127kxw72534w4u%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Retinopathy of prematurity (ROP) is a common blinding disease in children in the developed world despite current treatment,
 and is becoming increasingly prevalent in the developing world. ROP progresses in two phases. The first phase begins with
 delayed retinal vascular growth after birth and partial regression of existing vessels, followed by a second phase of hypoxia-induced
 pathological vessel growth. Two major risk factors of ROP are the use of oxygen and a decreased gestation period. Excessive
 oxygen contributes to ROP through regulation of vascular endothelial growth factor (VEGF). Suppression of VEGF by oxygen in
 phase I of ROP inhibits normal vessel growth, whereas elevated levels of VEGF induced by hypoxia in phase II of ROP precipitate
 pathological vesse...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778480</comments>
            <pubDate>Fri, 02 Mar 2007 08:54:55 +0100</pubDate>
            <guid isPermaLink="false">778480</guid>        </item>
        <item>
            <title>Development of the retinal vasculature</title>
            <link>http://www.medworm.com/index.php?rid=778481&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fw57036w56h87r117%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Blood vessels that supply the inner portion of the retina are extensively reorganized during development. The vessel regression,
 sprouting angiogenesis, vascular remodelling and vessel differentiation events involved critically depend on cell–cell signalling
 between different cellular components such as neurons, glia, endothelial cells, pericytes and immune cells. Studies in mice
 using transgenic and gene deletion approaches have started to unravel the genetic basis of some of these signalling pathways
 and have lead to a much improved understanding of the molecular mechanisms controlling retinal blood vessel behaviour both
 during development and under pathological conditions. Such insight will provide the basis of future therapeutic approaches
 aimed at manipulat...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778481</comments>
            <pubDate>Sat, 24 Feb 2007 08:40:35 +0100</pubDate>
            <guid isPermaLink="false">778481</guid>        </item>
        <item>
            <title>Effects of topical administration of 12-methyl tetradecanoic acid (12-MTA) on the development of corneal angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=778482&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F016r236087860002%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Corneal vascularisation is a potentially devastating occurrence that can cause blindness. Currently, treatments for this condition
 are limited. In these studies, we have investigated a novel inhibitor of angiogenesis, 12-methyl tetradecanoic acid (12-MTA),
 to treat corneal vascularisation in mouse models of corneal alkali injury and corneal Pseudomonas aeruginosa infection. The effectiveness of 12-MTA was compared to treatment with dexamethasone. 12-MTA was found to be at least as effective
 as dexamethasone in reducing the angiogenesis that occurs following alkali injury or P. aeruginosa infection of the cornea. The major effect of both 12-MTA and dexamethasone in these models was to reduce the linear incursion
 of new blood vessels into the central cornea. A signifi...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778482</comments>
            <pubDate>Tue, 13 Feb 2007 08:29:19 +0100</pubDate>
            <guid isPermaLink="false">778482</guid>        </item>
        <item>
            <title>Prophylactic naked DNA vaccination with the human vascular endothelial growth factor induces an anti-tumor response in C57Bl/6 mice</title>
            <link>http://www.medworm.com/index.php?rid=778483&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F325396t1n2844874%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Passive immunotherapy against soluble pro-angiogenic factors and/or their receptors in endothelial cells has become a promising
 approach in cancer therapeutics. There is also experimental evidence indicating that an active immunotherapy strategy directed
 towards these target molecules could also be effective. In this paper we show that it is possible to reduce tumor growth or
 increase the survival of tumor-bearing C57Bl/6 mice when animals are vaccinated with the human vascular endothelial growth
 factor (VEGF) isoform 121 gene (hVEGF121), and later challenged with melanoma or lung carcinoma tumor cells. Immunization was done with 10&amp;nbsp;μg DNA doses of the hVEGF121
 gene, which is highly homologous to its mouse counterpart, administered on a weekly basis using a p...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778483</comments>
            <pubDate>Fri, 02 Feb 2007 07:48:39 +0100</pubDate>
            <guid isPermaLink="false">778483</guid>        </item>
        <item>
            <title>Regulation of endothelial cell migration by amphiphiles—are changes in cell membrane physical properties involved?</title>
            <link>http://www.medworm.com/index.php?rid=778484&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F9536254164682085%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;Endothelial cell (EC) migration is an integral part of angiogenesis and a prerequisite for malignant tumor growth. Recent
 studies suggest that amphiphilic compounds can regulate migration of bovine aortic ECs by altering the physical properties
 of the cell membrane lipid bilayers. A number of structurally different amphiphiles thus regulate the migration in quantitative
 correlation with their effects on the plasma membrane microviscosity. Many amphiphiles that affect EC migration and angiogenesis
 alter the physical properties of lipid bilayers, suggesting that such a regulatory mechanism may be of general importance.
 To investigate this notion, we studied the effects of lysophospholipids that inhibit migration of bovine aortic ECs and decrease
 cell membrane microv...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778484</comments>
            <pubDate>Tue, 30 Jan 2007 07:38:17 +0100</pubDate>
            <guid isPermaLink="false">778484</guid>        </item>
        <item>
            <title>An intimate interplay between precocious, migrating pericytes and endothelial cells governs human fetal brain angiogenesis</title>
            <link>http://www.medworm.com/index.php?rid=778485&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fp65546664111h543%2F</link>
            <description>Abstract&amp;nbsp;&amp;nbsp;In order to better understand the process of angiogenesis in the developing human brain, we have examined the spatial relationship
 and relative contributions of endothelial cells and pericytes, the two primary cell types involved in vessel growth, together
 with their relation with the vascular basement membrane. Pericytes were immunolocalized through use of the specific markers
 nerve/glial antigen 2 (NG2) proteoglycan, endosialin (CD248) and the platelet-derived growth factor receptor β (PDGFR-β),
 while endothelial cells were identified by the pan-endothelial marker CD31 and the blood brain barrier (BBB)-specific markers
 claudin-5 and glucose transporter isoform 1 (GLUT-1). The quantitative analysis demonstrates that microvessels of the fetal
 human telencephalon...</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778485</comments>
            <pubDate>Wed, 17 Jan 2007 07:43:25 +0100</pubDate>
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        <item>
            <title>Elucidation of the mechanisms underlying the angiogenic effects of ginsenoside Rg1 in vivo and in vitro</title>
            <link>http://www.medworm.com/index.php?rid=778486&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2Fu461403443024x26%2F</link>
            <description>Without Abstract
	Content TypeJournal Article

	
		JournalAngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970
	
		Journal VolumeVolume 10
	
		Journal IssueVolume 10, Number 1 / March, 2007 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778486</comments>
            <pubDate>Thu, 07 Dec 2006 08:44:10 +0100</pubDate>
            <guid isPermaLink="false">778486</guid>        </item>
        <item>
            <title>Vascular development is disrupted by endothelial cell-specific expression of the anti-apoptotic protein Bcl-2</title>
            <link>http://www.medworm.com/index.php?rid=778487&amp;cid=s_35902_67_f&amp;fid=35902&amp;url=http%3A%2F%2Fwww.springerlink.com%2Fcontent%2F8rx4502131315t3u%2F</link>
            <description>This study provides direct experimental evidence that endothelial cell apoptosis plays an essential
 role during embryogenesis. Our results suggest that EC apoptosis plays an important role in determining the structure of the
 microcirculation but may be dispensable for large vessel development.
 
	Content TypeJournal Article

	
		JournalAngiogenesisOnline ISSN 1573-7209Print ISSN 0969-6970
	
		Journal VolumeVolume 10
	
		Journal IssueVolume 10, Number 1 / March, 2007 (Source: Angiogenesis)</description>
            <author>Angiogenesis</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=778487</comments>
            <pubDate>Wed, 06 Dec 2006 14:35:17 +0100</pubDate>
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