<?xml version="1.0" encoding="iso-8859-1"?>
<!-- generator="FeedCreator 1.7.2" -->
<rss version="2.0">
    <channel>
        <title>Journal of Cellular Physiology 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 'Journal of Cellular Physiology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Journal+of+Cellular+Physiology&t=Journal+of+Cellular+Physiology&s=Search&f=source]]></link>
        <lastBuildDate>Tue, 07 Feb 2012 08:48:58 +0100</lastBuildDate>
        <item>
            <title>Myeloid Elf‐1‐like factor stimulates adipogenic differentiation through the induction of peroxisome proliferator‐activated receptor γ expression in bone marrow</title>
            <link>http://www.medworm.com/index.php?rid=5658017&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24064</link>
            <description>AbstractMyeloid Elf‐1 like factor (MEF) is one of the Ets transcription factors known to regulate cell proliferation and differentiation. A previous report has shown that osteoblast‐specific MEF transgenic mice (Col1a1‐MEF‐TG mice) have low bone mass but high bone marrow adiposity. In the present study, we explored a previously unappreciated mechanism whereby MEF promotes adipogenesis in bone marrow. An adipogenic colony forming unit assay showed that bone marrow cells derived from Col1a1‐MEF‐TG mice had a higher adipogenic differentiation potential compared to those from wild‐type. The levels of adipogenic marker genes expression in 3T3L1 cells were higher when co‐cultured with Col1a1‐MEF‐ TG bone marrow cells than with wild‐type cells. MC3T3‐E1 preosteoblasts tr...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5658017</comments>
            <pubDate>Sat, 04 Feb 2012 13:48:58 +0100</pubDate>
            <guid isPermaLink="false">5658017</guid>        </item>
        <item>
            <title>Gadd45a and Gadd45b modulate innate immune functions of granulocytes and macrophages by differential regulation of p38 and JNK signaling</title>
            <link>http://www.medworm.com/index.php?rid=5658020&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24067</link>
            <description>This study shows that mice lacking either Gadd45a or Gadd45b are defective in the recruitment of granulocytes and macrophages to the intra‐peritoneal cavity following intra‐peritoneal administration of the bacterial cell‐wall PAMP lipopolysaccharide (LPS). Bone marrow (BM) derived granulocytes and macrophages lacking either Gadd45a or Gadd45b are shown to be impaired in their chemotactic response to LPS, as well as other inflammatory stimuli such as fMLP and IL‐8. Evidence was obtained also implicating Gadd45a and Gadd45b in other myeloid innate immune functions, including ROS production, phagocytosis, and adhesion. Gadd45a and Gadd45b activation of p38 kinase was implicated in the response of granulocytes to LPS mediated chemotaxis, whereas Gadd45a and Gadd45b curtailment of JNK a...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5658020</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5658020</guid>        </item>
        <item>
            <title>CIZ/NMP4 is expressed in B16 melanoma and forms a positive feedback loop with RANKL to promote migration of the melanoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5658019&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24066</link>
            <description>AbstractTumor metastasis to bone is a serious pathological situation that causes severe pain, and deterioration in locomoter function. However, the mechanisms underlying tumor metastasis is still incompletely understood. CIZ/NMP4 is a nucleocytoplasmic shuttling protein and its roles in tumor cells have not been known. We, therefore, hypothesized the role of CIZ/NMP4 in B16 melanoma cells that metastasize to bone. CIZ/NMP4 is expressed in B16 cells. The CIZ/NMP4 expression levels are correlated to the metastatic activity in divergent types of melanoma cells. Overexpression of CIZ/NMP4increased B16 cell migration in Trans‐well assay. Conversely, siRNA‐based knockdown of CIZ/NMP4 suppressed migratory activity of these cells. As RANKL promotes metastasis of tumor cells in bone, we teste...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5658019</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5658019</guid>        </item>
        <item>
            <title>PI3K‐independent AKT activation in cancers: A treasure trove for novel therapeutics</title>
            <link>http://www.medworm.com/index.php?rid=5658018&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24065</link>
            <description>AbstractAKT/PKB serine threonine kinase, a critical signaling molecule promoting cell growth and survival pathways, is frequently dysregulated in many cancers. Although phosphatidylinositol‐3‐OH kinase (PI3K), a lipid kinase, is well characterized as a major regulator of AKT activation in response to a variety of ligands, recent studies highlight a diverse group of tyrosine (Ack1/TNK2, Src, PTK6) and serine/threonine (TBK1, IKBKE, DNAPKcs) kinases that activate AKT directly to promote its pro‐proliferative signaling functions. While some of these alternate AKT activating kinases respond to growth factors, others respond to inflammatory and genotoxic stimuli. A common theme emerging from these studies is that aberrant or hyperactivation of these alternate kinases is often associated w...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5658018</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5658018</guid>        </item>
        <item>
            <title>Src modulates contractile vascular smooth muscle function via regulation of focal adhesions</title>
            <link>http://www.medworm.com/index.php?rid=5636836&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24062</link>
            <description>AbstractSrc is a known regulator of focal adhesion turnover in migrating cells; but, in contrast, Src is generally assumed to play little role in differentiated, contractile vascular smooth muscle (dVSM). The goal of the present study was to determine if Src‐family kinases regulate focal adhesion proteins and how this might affect contractility of non‐proliferative vascular smooth muscle. We demonstrate here, through the use of phosphotyrosine screening, deconvolution microscopy imaging, and differential centrifugation, that the activity of Src family kinases in aorta is regulated by the alpha agonist and vasoconstrictor phenylephrine, and leads to focal adhesion protein phosphorylation and remodeling in dVSM. Furthermore, Src inhibition via morpholino knockdown of Src or by the small ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5636836</comments>
            <pubDate>Sat, 28 Jan 2012 18:13:20 +0100</pubDate>
            <guid isPermaLink="false">5636836</guid>        </item>
        <item>
            <title>TGFß1 inhibits lymphatic endothelial cell differentiation from mouse embryonic stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5636837&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24063</link>
            <description>AbstractThe lymphatic vasculature is essential for the maintenance of tissue fluid, immune surveillance and dissemination of metastasis. Recently, several models for lymphatic vascular research and markers specific for lymphatic endothelium have been characterized. Despite these significant achievements, our understanding of the early lymphatic development is still rather limited. The purpose of the study was to further define early lymphatic differentiation regulatory pathways. In the present study, we have developed conditions leading to lymphatic endothelial cell differentiation under both serum‐rich and serum‐free conditions, using the coculture system of Flk‐1‐positive vascular precursors derived from murine embryonic stem (ES) cells grown on an OP9 stromal cell layer. In this...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5636837</comments>
            <pubDate>Fri, 27 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5636837</guid>        </item>
        <item>
            <title>Brain‐derived neurotrophic factor induces migration of endothelial cells through a TrkB–ERK–integrin αVβ3–FAK cascade</title>
            <link>http://www.medworm.com/index.php?rid=5626289&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22942</link>
            <description>In this study, we examined the influence of BDNF on migration in human microvascular endothelial cells (HMVECs), focusing on the effects on extracellular signal‐regulated kinase (ERK), integrin αVβ3, and focal adhesion kinase (FAK). The migration of endothelial cells was assessed with a modified Boyden chamber and a wound healing assay. The expression of integrin αVβ3 and the phosphorylation of ERK and FAK were analyzed by immunoblotting and immunofluorescence microscopy. BDNF (25 ng/ml) induced cell migration. PD98059, an ERK inhibitor, K252a, a specific inhibitor for TrkB, a high affinity receptor of BDNF, and an anti‐integrin αVβ3 antibody suppressed the BDNF‐induced migration. BDNF increased the levels of integrin αVβ3 and phosphorylated ERK1/2 and FAK. The ERK inhibito...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626289</comments>
            <pubDate>Wed, 25 Jan 2012 15:44:38 +0100</pubDate>
            <guid isPermaLink="false">5626289</guid>        </item>
        <item>
            <title>Angiotensin‐(1–7) decreases LPS‐induced inflammatory response in macrophages</title>
            <link>http://www.medworm.com/index.php?rid=5626288&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22940</link>
            <description>AbstractIt has been previously shown that besides its classical role in blood pressure control the renin–angiotensin system, mainly by action of angiotensin II on the AT1 receptor, exerts pro‐inflammatory effects such as by inducing the production of cytokines. More recently, alternative pathways to this system were described, such as binding of angiotensin‐(1–7) to receptor Mas, which was shown to counteract some of the effects evoked by activation of the angiotensin II–AT1 receptor axis. Here, by means of different molecular approaches we investigated the role of angiotensin‐(1–7) in modulating inflammatory responses triggered in mouse peritoneal macrophages. Our results show that receptor Mas transcripts were up‐regulated by eightfold in LPS‐induced macrophages. Intere...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626288</comments>
            <pubDate>Wed, 25 Jan 2012 15:44:37 +0100</pubDate>
            <guid isPermaLink="false">5626288</guid>        </item>
        <item>
            <title>Parathyroid hormone‐related protein is a hypertrophy factor for human mesangial cells: Implications for diabetic nephropathy</title>
            <link>http://www.medworm.com/index.php?rid=5626287&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22926</link>
            <description>AbstractHypertrophy of human mesangial cells (HMC) is among the earliest characteristics in patients with diabetic nephropathy (DN). Recently, we observed the upregulation of parathyroid hormone (PTH)‐related protein (PTHrP) in experimental DN, associated with renal hypertrophy. Herein, we first examined whether PTHrP was overexpressed in human DN, and next assessed the putative role of this protein on high glucose (HG)‐induced HMC hypertrophy. As previously found in mice, kidneys from diabetic patients showed an increased tubular and glomerular immunostaining for PTHrP. In HMC, HG medium increased PTHrP protein expression associated with the development of hypertrophy as assessed by cell protein content. This effect was also induced by PTHrP(1–36). HG and PTHrP(1–36)‐induced hyp...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626287</comments>
            <pubDate>Wed, 25 Jan 2012 15:44:17 +0100</pubDate>
            <guid isPermaLink="false">5626287</guid>        </item>
        <item>
            <title>Duplicated chromosomal fragments stabilize shortened telomeres in normal human IMR‐90 cells before transition to senescence</title>
            <link>http://www.medworm.com/index.php?rid=5626286&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22921</link>
            <description>AbstractTo assess why during in vitro aging of fibroblasts the maintenance of chromosomal stability is effective or occasionally fails, a detailed cytogenetic analysis was performed in normal human IMR‐90 fetal lung fibroblasts. The onset of senescence was inferred from proliferation activity, expression pattern of cell cycle regulating proteins, activity of β‐galactosidase, and morphological features. Over the period of proliferation, a moderate increase of non‐transmissible structural chromosomal aberrations was observed. In addition, using fluorescence in situ hybridization (mFISH and mBAND) techniques, we detected clonally expanding translocations in up to 70% of the analyzed metaphases, all involving one homolog of chromosome 9 as an acceptor. Notably, chromosomes are randomly ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626286</comments>
            <pubDate>Wed, 25 Jan 2012 15:44:11 +0100</pubDate>
            <guid isPermaLink="false">5626286</guid>        </item>
        <item>
            <title>Afadin controls p120‐catenin–ZO‐1 interactions leading to endothelial barrier enhancement by oxidized phospholipids</title>
            <link>http://www.medworm.com/index.php?rid=5626285&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22916</link>
            <description>This study examined a role of afadin in the OxPAPC‐induced enhancement of interactions between adherens junctions and tight junctions as a novel mechanism of endothelial cell (EC) barrier preservation. OxPAPC induced Rap1‐dependent afadin accumulation at the cell periphery and Rap1‐dependent afadin interaction with adherens junction and tight junction proteins p120‐catenin and ZO‐1, respectively. Afadin knockdown using siRNA or ectopic expression of afadin mutant lacking Rap1 GTPase binding domain suppressed OxPAPC‐induced EC barrier enhancement and abolished barrier protective effects of OxPAPC against thrombin‐induced EC permeability. Afadin knockdown also abolished protective effects of OxPAPC against ventilator‐induced lung injury in vivo. These results demonstrate for ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626285</comments>
            <pubDate>Wed, 25 Jan 2012 15:44:04 +0100</pubDate>
            <guid isPermaLink="false">5626285</guid>        </item>
        <item>
            <title>Immortalization and characterization of osteoblast cell lines generated from wild‐type and Nmp4‐null mouse bone marrow stromal cells using murine telomerase reverse transcriptase (mTERT)</title>
            <link>http://www.medworm.com/index.php?rid=5626284&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22915</link>
            <description>AbstractIntermittent parathyroid hormone (PTH) adds new bone to the osteoporotic skeleton; the transcription factor Nmp4/CIZ represses PTH‐induced bone formation in mice and as a consequence is a potential drug target for improving hormone clinical efficacy. To explore the impact of Nmp4/CIZ on osteoblast phenotype, we immortalized bone marrow stromal cells from wildtype (WT) and Nmp4‐knockout (KO) mice using murine telomerase reverse transcriptase. Clonal lines were initially chosen based on their positive staining for alkaline phosphatase and capacity for mineralization. Disabling Nmp4/CIZ had no gross impact on osteoblast phenotype development. WT and KO clones exhibited identical sustained growth, reduced population doubling times, extended maintenance of the mature osteoblast phen...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626284</comments>
            <pubDate>Wed, 25 Jan 2012 15:44:03 +0100</pubDate>
            <guid isPermaLink="false">5626284</guid>        </item>
        <item>
            <title>The calcineurin—nuclear factor of activated T cells signaling pathway mediates the effect of corticotropin releasing factor and urocortins on catecholamine synthesis</title>
            <link>http://www.medworm.com/index.php?rid=5626283&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22914</link>
            <description>In conclusion, our data suggest that CRF1 and CRF2 ligands activate the transcription factor NFAT and its activation is prerequisite for CRF‐induced catecholamine production from chromaffin cells. J. Cell. Physiol. 227: 1861–1872, 2012. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626283</comments>
            <pubDate>Wed, 25 Jan 2012 15:44:02 +0100</pubDate>
            <guid isPermaLink="false">5626283</guid>        </item>
        <item>
            <title>Acetylation‐dependent nuclear arrangement and recruitment of BMI1 protein to UV‐damaged chromatin</title>
            <link>http://www.medworm.com/index.php?rid=5626282&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22912</link>
            <description>AbstractPolycomb group (PcG) proteins, organized into Polycomb bodies, are important regulatory components of epigenetic processes involved in the heritable transcriptional repression of target genes. Here, we asked whether acetylation can influence the nuclear arrangement and function of the BMI1 protein, a core component of the Polycomb group complex, PRC1. We used time‐lapse confocal microscopy, micro‐irradiation by UV laser (355 nm) and GFP technology to study the dynamics and function of the BMI1 protein. We observed that BMI1 was recruited to UV‐damaged chromatin simultaneously with decreased lysine acetylation, followed by the recruitment of heterochromatin protein HP1β to micro‐irradiated regions. Pronounced recruitment of BMI1 was rapid, with half‐time τ = 15 s...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626282</comments>
            <pubDate>Wed, 25 Jan 2012 15:43:59 +0100</pubDate>
            <guid isPermaLink="false">5626282</guid>        </item>
        <item>
            <title>Zearalenone induces apoptosis and necrosis in porcine granulosa cells via a caspase‐3‐ and caspase‐9‐dependent mitochondrial signaling pathway</title>
            <link>http://www.medworm.com/index.php?rid=5626281&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22906</link>
            <description>This study thus offers a novel insight into molecular mechanisms by which zearalenone has adverse cytotoxicity on reproduction. J. Cell. Physiol. 227: 1814–1820, 2012. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626281</comments>
            <pubDate>Wed, 25 Jan 2012 15:43:55 +0100</pubDate>
            <guid isPermaLink="false">5626281</guid>        </item>
        <item>
            <title>Highlights: Volume 227, Number 5</title>
            <link>http://www.medworm.com/index.php?rid=5626280&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23962</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626280</comments>
            <pubDate>Wed, 25 Jan 2012 15:43:49 +0100</pubDate>
            <guid isPermaLink="false">5626280</guid>        </item>
        <item>
            <title>Table of Contents: Volume 227, Number 5</title>
            <link>http://www.medworm.com/index.php?rid=5626279&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23961</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626279</comments>
            <pubDate>Wed, 25 Jan 2012 15:43:48 +0100</pubDate>
            <guid isPermaLink="false">5626279</guid>        </item>
        <item>
            <title>Journal of Cellular Physiology: Volume 227, Number 5, May 2012</title>
            <link>http://www.medworm.com/index.php?rid=5626278&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23960</link>
            <description>AbstractCover: Telomere FISH and mFISH stained metaphase spread. See article in this issue by Zahnreich et al., pages 1932–1840.. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626278</comments>
            <pubDate>Wed, 25 Jan 2012 15:43:46 +0100</pubDate>
            <guid isPermaLink="false">5626278</guid>        </item>
        <item>
            <title>PAR‐1‐dependent and PAR‐independent pro‐inflammatory signalling in human lung fibroblasts exposed to thrombin</title>
            <link>http://www.medworm.com/index.php?rid=5636838&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24061</link>
            <description>We report that primary human lung fibroblasts secrete CCL2 in a PAR‐1‐dependent manner at low thrombin concentration (∼ 0.3 nM). At or above 10 nM thrombin, pharmacological antagonism (RWJ‐58259) fails to block thrombin‐induced CCL2 release; whereas PAR‐1 cleavage‐blocking monoclonal antibodies (ATAP2 and WEDE15) only partially inhibit thrombin‐induced CCL2 secretion. In addition, activation of PAR‐3, PAR‐4 and transactivation of either PAR‐2 or EGFR were ruled out as being responsible for thrombin‐mediated CCL2 secretion at high yet standard concentrations of the proteinase. We further provide evidence that PAR‐1‐dependent and PAR‐independent signaling involves the rapid phosphorylation of ERK which in turn is absolutely required for thrombin‐induced CCL2 s...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5636838</comments>
            <pubDate>Wed, 25 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5636838</guid>        </item>
        <item>
            <title>In silico analysis of the two tandem somatomedin B domains of ENPP1 reveals hints on the homodimerization of the protein</title>
            <link>http://www.medworm.com/index.php?rid=5605821&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24058</link>
            <description>AbstractThe homodimerization of ENPP1 is mediated by the two somatomedin B (SMB) domains of the protein through a mechanism that is yet unknown at the atomistic level. The tandem arrangement of these domains without an intermediate spacer implies their possible packing into a functional assembly, which we explored by rigid docking. To exclude potential bias in the docking search we assessed the absence of flexible protein regions by evaluating the normalized B‐factors calculated from the Ca atom displacements derived from Molecular Dynamics simulations. After filtering the docking results exploiting the criterion that residues located at the inter‐domain interfaces are more conserved than non‐interface residues, the resulting best model of the tandem SMB domains revealed the presence...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605821</comments>
            <pubDate>Thu, 19 Jan 2012 13:53:37 +0100</pubDate>
            <guid isPermaLink="false">5605821</guid>        </item>
        <item>
            <title>Report of the 2011 annual meeting of the Italian society for virology</title>
            <link>http://www.medworm.com/index.php?rid=5605825&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24055</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605825</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605825</guid>        </item>
        <item>
            <title>Metaboloepigenetics: Interrelationships between energy metabolism and epigenetic control of gene expression</title>
            <link>http://www.medworm.com/index.php?rid=5605824&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24054</link>
            <description>AbstractDiet and energy metabolism affect gene expression, which influences human health and disease. Here, we discuss the role of epigenetics as a mechanistic link between energy metabolism and control of gene expression. A number of key energy metabolites including SAM, acetyl‐CoA, NAD+, and ATP serve as essential co‐factors for many, perhaps most, epigenetic enzymes that regulate DNA methylation, posttranslational histone modifications, and nucleosome position. The relative abundance of these energy metabolites allows a cell to sense its energetic state. And as co‐factors, energy metabolites act as rheostats to modulate the activity of epigenetic enzymes and upregulate/downregulate transcription as appropriate to maintain homeostasis. J. Cell. Physiol. © 2012 Wiley Periodicals, I...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605824</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605824</guid>        </item>
        <item>
            <title>Inactivation of Bcl‐2 through IκB kinase (IKK)‐dependent phosphorylation mediates apoptosis upon exposure to 4‐hydroxynonenal (HNE)</title>
            <link>http://www.medworm.com/index.php?rid=5605823&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24057</link>
            <description>AbstractApoptosis of macrophage foam cells loaded with modified/oxidized lipids is implicated in destabilization of advanced atherosclerotic plaques in humans. Concentration of HNE, main aldehydic product of plasma LDL peroxidation, elevates in atherosclerotic lesions as well as in cultured cells under oxidative stress. Although this reactive aldehyde has been shown to promote apoptosis with the involvement of p38 MAPK and JNK in various mammalian cell lines, roles of Bcl‐2 family proteins remain to be deciphered. We demonstrated that HNE‐induced apoptosis was accompanied by concurrent downregulations of antiapoptotic Bcl‐xL and Mcl‐1 as well as upregulation of proapoptotic Bak. Furthermore phoshorylation of Bcl‐2 at Thr56, Ser70, and probably more phosphorylation sites located o...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605823</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605823</guid>        </item>
        <item>
            <title>Bone marrow stromal cells stimulate an angiogenic program that requires endothelial MT1‐MMP</title>
            <link>http://www.medworm.com/index.php?rid=5605822&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24056</link>
            <description>AbstractBone marrow‐derived stromal/stem cells (BMSCs) have recently been characterized as mediators of tissue regeneration after injury. In addition to preventing fibrosis at the wound site, BMSCs elicit an angiogenic response within the fibrin matrix. The mechanistic interactions between BMSCs and invading endothelial cells (ECs) during this process are not fully understood. Using a three‐dimensional, fibrin‐based angiogenesis model, we sought to investigate the proteolytic mechanisms by which BMSCs promote vessel morphogenesis. We find that BMSC‐mediated vessel formation depends on the proteolytic ability of membrane type 1‐matrix metalloproteinase (MT1‐MMP). Knockdown of the protease results in a small network of vessels with enlarged lumens. Contrastingly, vessel morphogen...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605822</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605822</guid>        </item>
        <item>
            <title>Osteoclastogenesis is negatively regulated by D‐serine produced by osteoblasts</title>
            <link>http://www.medworm.com/index.php?rid=5605831&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24048</link>
            <description>In this study, we evaluated the possible functional expression of SR by bone‐forming osteoblasts and bone‐resorbing osteoclasts. Expression of SR mRNA was seen in osteoblasts localized at the cancellous bone surface in neonatal rat tibial sections, and in cultured rat calvarial osteoblasts endowed to release D‐Ser into extracellular medium, but not in cultured osteoclasts differentiated from murine bone marrow progenitor cells. Sustained exposure to D‐Ser failed to significantly affect alkaline phosphatase activity and Ca2+ accumulation in cultured osteoblasts, but significantly inhibited differentiation and maturation in a concentration‐dependent manner at a concentration range of 0.1 to 1 mM without affecting cellular survival in cultured osteoclasts. By contrast, L‐Ser pro...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605831</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605831</guid>        </item>
        <item>
            <title>Biological effects of the plant‐derived polyphenol resveratrol in human articular cartilage and chondrosarcoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5605830&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24049</link>
            <description>AbstractThe natural phytoestrogen resveratrol (RSV) may have therapeutic potential for arthritic conditions.  RSV is chondroprotective for articular cartilage in rabbit models for arthritis, but its biological effects on human articular cartilage and chondrosarcoma cells are unknown. Effects of RSV on human articular cartilage homeostasis were studied by assessing production of matrix‐degrading enzymes (MMP‐13, ADAMTS‐4, and ADAMTS‐5), as well as proteoglycan production and synthesis. The counteractions of RSV against catabolic factors (e.g., FGF‐2 or IL‐1β) were examined by in vitro and ex vivo using monolayer, three‐dimensional alginate beads and cartilage explants cultures, respectively. RSV improves cell viability of articular chondrocytes and effectively antagonizes car...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605830</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605830</guid>        </item>
        <item>
            <title>JC virus load in cerebrospinal fluid and transcriptional control region rearrangements may predict the clinical course of progressive multifocal leukoencephalopathy</title>
            <link>http://www.medworm.com/index.php?rid=5605829&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24051</link>
            <description>AbstractProgressive multifocal leukoencephalopathy (PML) is a severe disease of the central nervous system (CNS), caused by infection with the Polyomavirus JC virus (JCV). Because there are no known treatments or prognostic factors, we performed a long‐term study focusing mainly on cerebrospinal fluid (CSF) samples from PML patients to describe the virological features akin to the different forms of the disease. Twenty‐eight PML patients were enrolled: 10 HIV‐1+ patients with classical PML (CPML), 9 HIV‐1+ patients with slowly progressing or stable neurological symptoms (benign PML), 3 HIV‐1+ asymptomatic patients and 6 HIV‐1‐negative patients. CSF, urine and blood samples were collected at the enrollment (baseline) and every six months afterwards when possible. The JCV DNA a...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605829</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605829</guid>        </item>
        <item>
            <title>Involvements of the ABC protein ABCF2 and α‐actinin‐4 in regulation of cell volume and anion channels in human epithelial cells</title>
            <link>http://www.medworm.com/index.php?rid=5605828&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24050</link>
            <description>AbstractAfter osmotic swelling, cell volume is regulated by a process called regulatory volume decrease (RVD). Although actin cytoskeletons are known to play a regulatory role in RVD, it is not clear how actin‐binding proteins are involved in the RVD process. In the present study, an involvement of an actin‐binding protein, α‐actinin‐4 (ACTN4), in RVD was examined in human epithelial HEK293T cells. Overexpression of ACTN4 significantly facilitated RVD, whereas siRNA‐mediated downregulation of endogenous ACTN4 suppressed RVD. When the cells were subjected to hypotonic stress, the content of ACTN4 increased in a 100,000 × g pellet, which was sensitive to cytochalasin D pretreatment. Protein overlay assays revealed that ABCF2, a cytosolic member of the ABC transporter superfam...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605828</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605828</guid>        </item>
        <item>
            <title>Biogenesis, functions and fate of plant microRNAs</title>
            <link>http://www.medworm.com/index.php?rid=5605827&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24052</link>
            <description>AbstractMicroRNAs (miRNAs), a recently discovered class of small RNAs, are endogenously transcribed non‐coding RNAs that are known to control diverse developmental processes and defense responses. They regulate these pathways by fine‐tuning the levels of transcripts to which they bind and cause their cleavage or translation repression. Several studies on the processing of miRNA precursors have shed light on the essential structural features for precise release of miRNA duplexes. The identification of a protein that degrade single stranded small RNA has provided us with some understanding of how miRNA flux is maintained in plants. This review focuses on the genome organization, biogenesis, miRNA activity and the fate of miRNAs. J. Cell. Physiol. © 2012 Wiley Periodicals, Inc. (Source: ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605827</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605827</guid>        </item>
        <item>
            <title>Phenylephrine protects cardiomyocytes from starvation‐ induced apoptosis by increasing Glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) activity</title>
            <link>http://www.medworm.com/index.php?rid=5605826&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24053</link>
            <description>In conclusion, the present study provides the first direct evidence of an antiapoptotic role of GAPDH in PE‐induced cardiomyocytes protection; GAPDH activity elevation mainly affects the mitochondria‐induced apoptosis. J. Cell. Physiol. © 2012 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5605826</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5605826</guid>        </item>
        <item>
            <title>Requirements for ion and solute transport, and pH regulation during enamel maturation</title>
            <link>http://www.medworm.com/index.php?rid=5579210&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22911</link>
            <description>AbstractTranscellular bicarbonate transport is suspected to be an important pathway used by ameloblasts to regulate extracellular pH and support crystal growth during enamel maturation. Proteins that play a role in amelogenesis include members of the ABC transporters (SLC gene family and CFTR). A number of carbonic anhydrases (CAs) have also been identified. The defined functions of these genes are likely interlinked during enamel mineralization. The purpose of this study is to quantify relative mRNA levels of individual SLC, Cftr, and CAs in enamel cells obtained from secretory and maturation stages on rat incisors. We also present novel data on the enamel phenotypes for two animal models, a mutant porcine (CFTR‐ΔF508) and the NBCe1‐null mouse. Our data show that two SLCs (AE2 and NB...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579210</comments>
            <pubDate>Thu, 12 Jan 2012 12:47:45 +0100</pubDate>
            <guid isPermaLink="false">5579210</guid>        </item>
        <item>
            <title>Mapping the zinc‐transporting system in mammary cells: Molecular analysis reveals a phenotype‐dependent zinc‐transporting network during lactation</title>
            <link>http://www.medworm.com/index.php?rid=5579209&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22900</link>
            <description>AbstractThe mammary epithelial cell transitions from a non‐secreting to a terminally differentiated, secreting cell during lactation. Zinc (Zn) is a key modulator of phenotypic transition as it regulates over 300 biological functions including transcription, translation, energy transformation, intracellular signaling, and apoptosis. In addition, Zn must be redirected from normal cellular functions into the secretory compartment, as many components of the secretory system are Zn‐dependent and an extraordinary amount of Zn is secreted (1–3 mg Zn/day) into milk. Herein, we utilized a “systems biology” approach of genomic and proteomic profiling to explore mechanisms through which Zn is reallocated during phenotype transition in the lactating mammary gland from mice and cultured ma...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579209</comments>
            <pubDate>Thu, 12 Jan 2012 12:47:43 +0100</pubDate>
            <guid isPermaLink="false">5579209</guid>        </item>
        <item>
            <title>Comparison of the skeletal effects induced by daily administration of PTHrP (1–36) and PTHrP (107–139) to ovariectomized mice</title>
            <link>http://www.medworm.com/index.php?rid=5579208&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22902</link>
            <description>AbstractWe here compared the changes induced by subcutaneous injection of PTHrP (1–36) or PTHrP (107–139) (80 µg/kg/day, 5 days/week for 4 or 8 weeks) in bone histology and bone remodeling factors, and in bone marrow cells (BMCs) ex vivo, in ovariectomized (OVX) mice. We also examined the osteogenic effects of these peptides in mouse mesenchymal C3H10T1/2 cells under oxidative stress condition in vitro, which recapitulates the effects of OVX. We confirmed that PTHrP (1–36) exerts bone anabolic actions, as assessed by bone histology and osteoblast differentiation markers in the long bones and plasma from OVX mice. PTHrP (107–139) was also efficient in stimulating several bone formation parameters, and it dramatically decreased bone resorption markers. Moreover, both PTHrP pepti...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579208</comments>
            <pubDate>Thu, 12 Jan 2012 12:47:41 +0100</pubDate>
            <guid isPermaLink="false">5579208</guid>        </item>
        <item>
            <title>Inhibition of lung cancer growth: ATP citrate lyase knockdown and statin treatment leads to dual blockade of mitogen‐activated protein Kinase (MAPK) and Phosphatidylinositol‐3‐kinase (PI3K)/AKT pathways</title>
            <link>http://www.medworm.com/index.php?rid=5579207&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22895</link>
            <description>AbstractATP citrate lyase (ACL) catalyzes the conversion of cytosolic citrate to acetyl‐CoA and oxaloacetate. A definitive role for ACL in tumorigenesis has emerged from ACL RNAi and chemical inhibitor studies, showing that ACL inhibition limits tumor cell proliferation and survival and induces differentiation in vitro. In vivo, it reduces tumor growth leading to a cytostatic effect and induces differentiation. However, the underlying molecular mechanisms are poorly understood and agents that could enhance the efficacy of ACL inhibition have not been identified. Our studies focus on non‐small cell lung cancer (NSCLC) lines, which show phosphatidylinositol 3‐kinase (PI3K)/AKT activation secondary to a mutation in the K‐Ras gene or the EGFR gene. Here we show that ACL knockdown promo...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579207</comments>
            <pubDate>Thu, 12 Jan 2012 12:47:37 +0100</pubDate>
            <guid isPermaLink="false">5579207</guid>        </item>
        <item>
            <title>Cellular and molecular large‐scale features of fetal adipose tissue: Is bovine perirenal adipose tissue Brown1685</title>
            <link>http://www.medworm.com/index.php?rid=5579206&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22893</link>
            <description>AbstractEpidemiological and fetal programming studies point to the role of fetal growth in adult adipose tissue (AT) mass in large mammals. Despite the incidence of fetal AT growth for human health and animal production outcomes, there is still a lack of relevant studies. We determined the cellular and large‐scale‐molecular features of bovine fetal perirenal AT sampled at 110, 180, 210, and 260 days post‐conception (dpc) with the aim of identifying key cellular and molecular events in AT growth. The increase in AT weight from 110 to 260 dpc resulted from an increase in adipocyte volume and particularly adipocyte number that were concomitant with temporal changes in the abundance of 142 proteins revealed by proteomics. At 110 and 180 dpc, we identified proteins such as TCP1, FKBP4...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579206</comments>
            <pubDate>Thu, 12 Jan 2012 12:47:34 +0100</pubDate>
            <guid isPermaLink="false">5579206</guid>        </item>
        <item>
            <title>Pharmacokinetic analysis of plasma curves obtained after i.v. injection of the PET radioligand [11C] raclopride provides a likely explanation for rapid radioligand metabolism</title>
            <link>http://www.medworm.com/index.php?rid=5579205&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22890</link>
            <description>AbstractPositron emission tomography (PET) is an imaging technique that provides direct measurements of receptor binding in neurons. The present study was performed to find reasons for the common observation of rapid metabolism of receptor radioligands during time of a brain PET scan. To this aim, the 1‐h phase during which imaging‐data are acquired was evaluated by using a pharmacokinetic approach. The values of half‐lives, volumes of distribution, and dilution calculated for a set of metabolite corrected plasma curves of D2‐receptor radioligand [11C]raclopride (PETc) during 50 min after radioligand injection in tracer dose were compared with the reference values obtained from a set of plasma curves (REFc) during 30 h after i.v. infusion of unlabelled raclopride in pharmacolog...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579205</comments>
            <pubDate>Thu, 12 Jan 2012 12:47:31 +0100</pubDate>
            <guid isPermaLink="false">5579205</guid>        </item>
        <item>
            <title>Embryologic origin of endometriosis: Analysis of 101 human female fetuses</title>
            <link>http://www.medworm.com/index.php?rid=5579204&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22888</link>
            <description>AbstractThe etiology of endometriosis, a gynecological disease characterized by the presence of endometrial glands and stroma outside the uterine cavity, is still unknown. Our research group has recently demonstrated the presence of ectopic endometrium in human female fetuses at different gestational ages. In this manuscript we describe four new cases of fetal endometriosis found among a series of 52 female fetuses analyzed at autopsy. The anatomical localization of this ectopic endometrium, and its histological and immunohistochemical characteristics are depicted. We suggest that endometriosis is caused by dislocation of primitive endometrial tissue outside the uterine cavity during organogenesis. The clinical and pathological implications of these findings are discussed. J. Cell. Physiol...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579204</comments>
            <pubDate>Thu, 12 Jan 2012 12:47:29 +0100</pubDate>
            <guid isPermaLink="false">5579204</guid>        </item>
        <item>
            <title>Interplay between membrane lipid peroxidation, transglutaminase activity, and Cyclooxygenase 2 expression in the tissue adjoining to breast cancer</title>
            <link>http://www.medworm.com/index.php?rid=5579203&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22874</link>
            <description>AbstractBreast cancer, a leading cause of cancer related deaths worldwide, is one of the most common neoplasms in women. The increased generation of reactive oxygen species (ROS) in breast lesion is critically involved in the mutagenic processes that drive to breast carcinoma initiation and progression. To date, the molecular events occurring in the tissue adjoin the cancer lesion have not been elucidated. Here, we investigated the role of excess ROS generation during human breast carcinogenesis by evaluating oxidative stress biomarkers, tissue transglutaminase (t‐TGase) activity, and expression levels of ubiquitin and cyclooxygenase‐2 (COX‐2) in the normal tissue adjoin to fibroadenoma (nFA), atypical ductal hyperplasia (nADH), and invasive ductal carcinoma (nIDC) from 45 breast can...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579203</comments>
            <pubDate>Thu, 12 Jan 2012 12:47:18 +0100</pubDate>
            <guid isPermaLink="false">5579203</guid>        </item>
        <item>
            <title>Clozapine impairs insulin action by up‐regulating akt phosphorylation and Ped/Pea‐15 protein abundance</title>
            <link>http://www.medworm.com/index.php?rid=5579202&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22864</link>
            <description>AbstractClinical and experimental evidence indicates that atypical antipsychotics impair glucose metabolism. We investigated whether clozapine may directly affect insulin action by analyzing insulin signaling in vitro and in vivo. Clozapine reduced insulin‐stimulated glucose uptake in PC12 and in L6 cells, representative models of neuron and skeletal muscle, respectively. Consistently, clozapine reduced insulin effect on insulin receptor (IR) by 40% and on IR substrate‐1 (IRS1) tyrosine phosphorylation by 60%. Insulin‐stimulated Akt phosphorylation was also reduced by about 40%. Moreover, insulin‐dependent phosphorylation of protein kinase C‐ζ (PKC‐ζ) was completely blunted in clozapine‐treated cells. Interestingly, clozapine treatment was accompanied by an insulin‐indepe...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579202</comments>
            <pubDate>Thu, 12 Jan 2012 12:47:06 +0100</pubDate>
            <guid isPermaLink="false">5579202</guid>        </item>
        <item>
            <title>Hyposmotic stress causes ATP release and stimulates Na,K‐ATPase activity in porcine lens</title>
            <link>http://www.medworm.com/index.php?rid=5579201&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22858</link>
            <description>AbstractPurinergic receptors in lens epithelium suggest lens function can be altered by chemical signals from aqueous humor or the lens itself. Here we show release of ATP by intact porcine lenses exposed to hyposmotic solution (200 mOsm). 18α‐glycyrrhetinic acid (AGA) added together with probenecid eliminated the ATP increase. N‐ethylmaleimide (200 µM), an exocytotic inhibitor, had no significant effect on ATP increase. Lenses exposed to hyposmotic solution displayed a ∼400% increase of propidium iodide (PI) entry into the epithelium. The increased ability of PI (MW 668) to enter the epithelium suggests possible opening of connexin and/or pannexin hemichannels. This is consistent with detection of connexin 43, connexin 50, and pannexin 1 in the epithelium and the ability of AG...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579201</comments>
            <pubDate>Thu, 12 Jan 2012 12:46:59 +0100</pubDate>
            <guid isPermaLink="false">5579201</guid>        </item>
        <item>
            <title>Mechanisms controlling neurite outgrowth in a pheochromocytoma cell line: The role of TRPC channels</title>
            <link>http://www.medworm.com/index.php?rid=5579200&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22855</link>
            <description>AbstractTransient Receptor Potential Canonical (TRPC) channels are implicated in modulating neurite outgrowth. The expression pattern of TRPCs changes significantly during brain development, suggesting that fine‐tuning TRPC expression may be important for orchestrating neuritogenesis. To study how alterations in the TRPC expression pattern affect neurite outgrowth, we used nerve growth factor (NGF)‐differentiated rat pheochromocytoma 12 (PC12) cells, a model system for neuritogenesis. In PC12 cells, NGF markedly up‐regulated TRPC1 and TRPC6 expression, but down‐regulated TRPC5 expression while promoting neurite outgrowth. Overexpression of TRPC1 augmented, whereas TRPC5 overexpression decelerated NGF‐induced neurite outgrowth. Conversely, shRNA‐mediated knockdown of TRPC1 decre...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579200</comments>
            <pubDate>Thu, 12 Jan 2012 12:46:56 +0100</pubDate>
            <guid isPermaLink="false">5579200</guid>        </item>
        <item>
            <title>Highlights: Volume 227, Number 4</title>
            <link>http://www.medworm.com/index.php?rid=5579199&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23959</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579199</comments>
            <pubDate>Thu, 12 Jan 2012 12:46:38 +0100</pubDate>
            <guid isPermaLink="false">5579199</guid>        </item>
        <item>
            <title>Table of Contents: Volume 227, Number 4</title>
            <link>http://www.medworm.com/index.php?rid=5579198&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23958</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579198</comments>
            <pubDate>Thu, 12 Jan 2012 12:46:36 +0100</pubDate>
            <guid isPermaLink="false">5579198</guid>        </item>
        <item>
            <title>Journal of Cellular Physiology: Volume 227, Number 4, April 2012</title>
            <link>http://www.medworm.com/index.php?rid=5579197&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23957</link>
            <description>AbstractCover: The cover shows eat‐me signals and phagocytic receptors for the engulfment of apoptotic cells. See article in this issue by Wei Li, pages 1291‐1297. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579197</comments>
            <pubDate>Thu, 12 Jan 2012 12:46:35 +0100</pubDate>
            <guid isPermaLink="false">5579197</guid>        </item>
        <item>
            <title>The effect of exogenous histone H1 on rat adipose‐derived stem cell proliferation, migration, and osteogenic differentiation in vitro</title>
            <link>http://www.medworm.com/index.php?rid=5550818&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24042</link>
            <description>AbstractAdipose‐derived stem cells (ASCs) are of great interest for the development of novel cell therapies due to their ease of isolation and expansion, immunosuppressive activity and multilineage differentiation potential. However, the mechanisms underlying the therapeutic potential of ASCs remain to be elucidated. Others and we have shown that nuclear proteins such as histone H1 and high mobility group box 1 (HMGB1) play important roles in the maturation of dendritic cells (DCs). Furthermore, we previously demonstrated translocation of histone H1 from the nucleus to the cytoplasm and activation of mitogen‐activated protein kinases (MAPKs) in DCs. In the present study, we confirmed that histone H1 does not alter the immunophenotype and immunosuppression potential of ASCs, but that hi...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550818</comments>
            <pubDate>Fri, 30 Dec 2011 09:51:32 +0100</pubDate>
            <guid isPermaLink="false">5550818</guid>        </item>
        <item>
            <title>“Annexin A1: Novel roles in skeletal muscle biology”</title>
            <link>http://www.medworm.com/index.php?rid=5550833&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24032</link>
            <description>AbstractAnnexin A1 (ANXA1, lipocortin‐1) is the first characterized member of the annexin superfamily of proteins, so called since their main property is to bind (i.e. to annex) to cellular membranes in a Ca2+‐dependent manner. ANXA1 has been involved in a broad range of molecular and cellular processes, including anti‐inflammatory signalling, kinase activities in signal transduction, maintenance of cytoskeleton and extracellular matrix integrity, tissue growth, apoptosis and differentiation. New insights show that endogenous ANXA1 positively modulates myoblast cell differentiation by promoting migration of satellite cells and, consequently, skeletal muscle differentiation. This suggests that ANXA1 may contribute to the regeneration of skeletal muscle tissue and may have therapeutic ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550833</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550833</guid>        </item>
        <item>
            <title>Novel anti‐ErbB3 monoclonal antibodies show therapeutic efficacy in xenografted and spontaneous mouse tumors</title>
            <link>http://www.medworm.com/index.php?rid=5550832&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24037</link>
            <description>In this study, we have utilized DNA electroporation (DNA‐EP) to generate a set of novel hybridomas directed against human ErbB3, which have been characterized for their biochemical and functional properties and selected for their ability to negatively regulate the ErbB3‐mediated signaling pathway. In vitro, the anti‐ErbB3 antibodies modulate the growth rate of cancer cells of different origins. In vivo they show antitumoral properties in a xenograft model of human pancreatic tumor and in the ErbB2‐driven carcinogenesis genetically engineered mouse model (GEMM) for mammary tumor, the BALB/neuT. Our data confirm that downregulating the ErbB3‐mediated signals with the use of anti‐ErbB3 monoclonal antibodies is both feasible and relevant for therapeutic purposes and provides new op...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550832</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550832</guid>        </item>
        <item>
            <title>Inactivation of Ink4a/Arf leads to deregulated expression of miRNAs in K‐Ras transgenic mouse model of pancreatic cancer</title>
            <link>http://www.medworm.com/index.php?rid=5550831&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24036</link>
            <description>AbstractHuman Pancreatic Cancer (PC) is an aggressive disease, which has been recapitulated in transgenic animal model that provides unique opportunity for mechanistic understanding of disease progression and also for testing the efficacy of novel therapeutics. Emerging evidence suggests deregulated expression of microRNAs (miRNAs) in human PC, and thus we investigated the expression of miRNAs in pancreas tissues obtained from transgenic mouse models of K‐Ras (K), Pdx1‐Cre (C), K‐Ras;Pdx1‐Cre (KC) and K‐Ras;Pdx1‐Cre;INK4a/Arf (KCI), initially from pooled RNA samples using miRNA profiling, and further confirmed in individual specimens by quantitative RT‐PCR. We found over‐expression of miR‐21, miR‐221, miR‐27a, miR‐27b and miR‐155, and down‐regulation of miR‐21...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550831</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550831</guid>        </item>
        <item>
            <title>Wnt3a stimulates Mepe, matrix extracellular phosphoglycoprotein, expression directly by the activation of the canonical Wnt signaling pathway and indirectly through the stimulation of autocrine Bmp‐2 expression</title>
            <link>http://www.medworm.com/index.php?rid=5550830&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24038</link>
            <description>AbstractMatrix extracellular phosphoglycoprotein (MEPE) is a specific marker of mineralizing osteoblasts and osteocytes. Canonical BMP and Wnt signaling pathways are two of the strongest paracrine signals stimulating osteogenesis. Our previous results indicated that Mepe expression is stimulated by the BMP‐2‐signaling pathway. The specific aim of this study addressed whether Mepe expression is also controlled by Wnt signaling, and whether there is a cross‐regulation between two major osteogenic signaling pathways. Treatment with Wnt3a, a canonical Wnt signaling stimulator, strongly enhanced Mepe mRNA expression. Knock‐down of β‐catenin with siRNA completely reversed Wnt3a‐stimulated Mepe expression. The Mepe mRNA expression level was increased by overexpression of β‐catenin...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550830</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550830</guid>        </item>
        <item>
            <title>Oldenlandia Diffusa extracts exert antiproliferative and apoptotic effects on human breast cancer cells through ERα/Sp1‐mediated p53 activation</title>
            <link>http://www.medworm.com/index.php?rid=5550829&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24035</link>
            <description>AbstractBreast cancer is the most frequent tumor and a major cause of death among women. Estrogens play a crucial role in breast tumor growth, which is the rationale for the use of hormonal antiestrogen therapies. Unfortunately, not all therapeutic modalities are efficacious and it is imperative to develop new effective antitumoral drugs. Oldenlandia Diffusa (OD) is a well‐known medicinal plant used to prevent and treat many disorders, especially cancers. The aim of this study was to investigate the effects of OD extracts on breast cancer cell proliferation. We observed that OD extracts strongly inhibited anchorage‐dependent and –independent cell growth and induced apoptosis in Estrogen Receptor alpha (ERα)‐positive breast cancer cells, whereas proliferation and apoptotic response...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550829</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550829</guid>        </item>
        <item>
            <title>Biochemical and proteomic characterization of alkaptonuric chondrocytes</title>
            <link>http://www.medworm.com/index.php?rid=5550828&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24033</link>
            <description>AbstractAlkaptonuria (AKU) is a rare genetic disease associated with the accumulation of homogentisic acid (HGA) and its oxidized/polymerized products which leads to the deposition of melanin‐like pigments (ochronosis) in connective tissues. Although numerous case reports have described ochronosis in joints, little is known on the molecular mechanisms leading to such a phenomenon. For this reason, we characterized biochemically chondrocytes isolated from the ochronotic cartilage of AKU patients. Based on the macroscopic appearance of the ochronotic cartilage, two sub‐populations were identified: cells coming from the black portion of the cartilage were referred to as ‘black’ AKU chondrocytes, while those coming from the white portion were referred to as ‘white’ AKU chondrocytes...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550828</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550828</guid>        </item>
        <item>
            <title>Caveolin‐1 overexpression is associated with simultaneous abnormal expression of the E‐cadherin/α‐β catenins complex and multiple ErbB receptors and with lymph nodes metastasis in head and neck squamous cell carcinomas</title>
            <link>http://www.medworm.com/index.php?rid=5550827&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24034</link>
            <description>In this study we used 57 HNSCC specimens to investigate whether the abnormal expression of caveolin‐1 was associated with the derangement of the E‐cadherin‐catenins complex and with the overexpression of ErbB receptors. We demonstrate that in HNSCCs caveolin‐1 overexpression is associated with the simultaneous abnormal expression of at least one member of the E‐cadherin/α‐β catenins complex and multiple ErbB receptors as well as with lymph node metastases. We also demonstrate that chronic stimulation of a human hypopharyngeal carcinoma cell line (FaDu) with EGF induced the internalization of β‐catenin and caveolin‐1 and their co‐localization with EGFR. Moreover, EGF treatment induced an increased physical interaction between EGFR/β‐catenin/caveolin‐1 and between E...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550827</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550827</guid>        </item>
        <item>
            <title>Mechanisms of cytosolic targeting of matrix metalloproteinase‐2</title>
            <link>http://www.medworm.com/index.php?rid=5550826&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24040</link>
            <description>AbstractMatrix metalloproteinase‐2 (MMP‐2) is best understood for its biological actions outside the cell. However, MMP‐2 also localizes to intracellular compartments and the cytosol where it has several substrates, including troponin I (TnI). Despite a growing list of cytosolic substrates, we currently do not know the mechanism(s) that give rise to the equilibrium between intracellular and secreted MMP‐2 moieties. Therefore, we explored how cells achieve the unique distribution of this protease. Our data show that endogenous MMP‐2 targets inefficiently to the endoplasmic reticulum (ER) and shows significant amounts in the cytosol. Transfection of canonical MMP‐2 essentially reproduces this targeting pattern, suggesting it is the quality of MMP‐2 signal sequence that predomin...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550826</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550826</guid>        </item>
        <item>
            <title>Organosulfur derivatives of the HDAC inhibitor valproic acid sensitize human lung cancer cell lines to apoptosis and to cisplatin cytotoxicity</title>
            <link>http://www.medworm.com/index.php?rid=5550825&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24039</link>
            <description>AbstractLung cancer is the leading cause of cancer mortality worldwide and despite efforts made to improve clinical results, continuing poor survival rates indicate that novel therapeutic approaches are needed. Valproic acid (VPA), a short‐chain branched fatty acid used mainly for the treatment of epilepsy and bipolar disorder, has been shown to inhibit class I histone deacetylases (HDAC‐I), a group of enzymes involved in chromatin remodelling and which are thought to play a role in tumor development. Although evidence of VPA's therapeutic efficacy has also been observed in patients with solid tumors, the very high concentration required to induce antitumor activity limits its clinical usefulness. We used a panel of NSCLC cell lines to evaluate the activity and mechanisms of action of ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550825</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550825</guid>        </item>
        <item>
            <title>VE‐cadherin trans‐interactions modulate Rac activation and enhancement of lung endothelial barrier by iloprost</title>
            <link>http://www.medworm.com/index.php?rid=5550824&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24041</link>
            <description>This study utilized complementary approaches including siRNA knockdown, culturing in Ca2+‐free medium, and VE‐cadherin blocking antibody to alter VE‐cadherin extracellular interactions to investigate the role of VE‐cadherin outside‐in signaling in modulation of Rac activation and EC barrier regulation by prostacyclin analog iloprost. Spatial analysis of Rac activation in pulmonary EC by FRET revealed additional spike in iloprost‐induced Rac activity at the sites of newly formed cell‐cell junctions. In contrast, disruption of VE‐cadherin extracellular trans‐interactions suppressed iloprost‐activated Rac signaling and attenuated EC barrier enhancement and cytoskeletal remodeling. These inhibitory effects were associated with decreased membrane accumulation and activation ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550824</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550824</guid>        </item>
        <item>
            <title>Cardiac and skeletal muscle expression of mutant β‐myosin heavy chains, degree of functional impairment and phenotypic heterogeneity in hypertrophic cardiomyopathy</title>
            <link>http://www.medworm.com/index.php?rid=5550823&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24047</link>
            <description>In this study, the expression of the mutant β‐myosin protein isoform, isolated from slow‐twitch fibres of skeletal muscle, was demonstrated by Northern and Western blot analysis; this myosin showed a decreased in vitro motility activity and produced a lower actin‐activated ATPase activity. Isometric tension, measured in single slow‐twitch fibres isolated from the affected individuals, also showed a significant decrease. The degree of impairment of β‐myosin function, as well as the loss in isometric tension development, were strictly dependent on the amount of the isoform transcribed from the mutated allele. Interestingly, a strong correlation was also demonstrated between mutant β‐myosin content and clinical features of FHC. On the other hand, we were unable to detect any co...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550823</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550823</guid>        </item>
        <item>
            <title>Agonist‐activated Ca2+ influx and Ca2+‐dependent Cl− channels in xenopus ovarian follicular cells: functional heterogeneity within the cell monolayer</title>
            <link>http://www.medworm.com/index.php?rid=5550822&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24046</link>
            <description>AbstractXenopus follicles are endowed with specific receptors for ATP, ACh, and AII, transmitters proposed as follicular modulators of gamete growth and maturation in several species. Here, we studied ion‐current responses elicited by stimulation of these receptors and their activation mechanisms using the voltage‐clamp technique. All agonists elicited Cl‐ currents that depended on coupling between oocyte and follicular cells and on an increase in intracellular Ca2+ concentration ([Ca2+]i), but they differed in their activation mechanisms and in the localization of the molecules involved. Both ATP and ACh generated fast Cl‐ (FCl) currents, while AII activated an oscillatory response; a robust Ca2+ influx linked specifically to FCl activation elicited an inward current (Iiw,Ca) whic...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550822</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550822</guid>        </item>
        <item>
            <title>Targeting Runx2 expression in hypertrophic chondrocytes impairs endochondral ossification during early skeletal development</title>
            <link>http://www.medworm.com/index.php?rid=5550821&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24045</link>
            <description>AbstractRunx2 is a known master transcription factor for osteoblast differentiation, as well as an essential regulator for chondrocyte maturation. Recently, more and more data has shown that Runx2 regulates hypertrophic chondrocyte‐specific type X collagen gene (Col10a1) expression in different species. However, how Runx2 regulation of Col10a1 expression impacts chondrocyte maturation, an essential step of endochondral bone formation, remains unknown. We have recently generated transgenic mice in which flag‐tagged Runx2 was driven by a cell‐specific Col10a1 control element. Significantly increased level of Runx2 and Col10a1 mRNA transcripts were detected in transgenic mouse limbs at both E17.5 (embryonic day 17.5) and P1 (postnatal day1) stages, suggesting an in vivo correlation of R...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550821</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550821</guid>        </item>
        <item>
            <title>Effect of 17β–estradiol and flavonoids on the regulation of expression of newly identified estrogen responsive genes in a rat raphe nuclei–derived cell line</title>
            <link>http://www.medworm.com/index.php?rid=5550820&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24044</link>
            <description>AbstractDue to the health risks attributed to perimenopausal hormone therapy, phytoestrogens such as flavonoids are receiving widespread attention to help alleviate menopausal symptoms, including hormone–driven mood disorders. Based on our previous reporter gene study regarding their transactivational activity in raphe nuclei cells from a brain region involved in regulation of mood disturbances, we herein study their effects on the regulation of expression of 17β–Estradiol (E2)–regulated genes. DNA microarray was used to globally assess E2–induced gene expression in RNDA cells, a rat raphe nuclei–derived cellular model expressing estrogen receptor β. Out of 212 regulated genes, six were selected for verification and as endpoints for the effect of flavonoids on the regulation of...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550820</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550820</guid>        </item>
        <item>
            <title>Scriptaid effects on breast cancer cell lines</title>
            <link>http://www.medworm.com/index.php?rid=5550819&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24043</link>
            <description>AbstractIn breast cancer tumor expression of estrogen receptors (ERs) is important as a marker of prognosis and mostly as a predictor of response to endocrine therapy. In fact, the loss of α‐ER expression leads to unresponsiveness to anti‐hormone treatment. In a significant fraction of breast cancers, this loss of expression is a result of epigenetic mechanisms, such as DNA methylation and histone deacetylation, within the α‐ER promoter. Previous studies have shown that pharmacologic inhibition of these mechanisms using the DNA methyltransferase inhibitor, 5‐aza‐2‐deoxycytidine (AZA), and the histone deacetylase (HDAC) inhibitor, Trichostatin A (TSA), results in expression of functional α‐ER mRNA and protein. Moreover, the activity of a novel HDAC inhibitor, Scriptaid, has...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550819</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5550819</guid>        </item>
        <item>
            <title>Pathophysiology of stroke and stroke‐induced retinal ischemia: Emerging role of stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5535497&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23048</link>
            <description>AbstractThe current review focuses on pathophysiology, animal models and molecular analysis of stroke and retinal ischemia, and the role of stem cells in recovery of these disease conditions. Research findings associated with ischemic stroke and retinal ischemia have been discussed, and efforts towards prevention and limiting the recurrence of ischemic diseases, as well as emerging treatment possibilities with endothelial progenitor cells (EPCs) in ischemic diseases, are presented. Although most neurological diseases are still not completely understood and reliable treatment is lacking, animal models provide a major step in validating novel therapies. Stem cell approaches constitute an emerging form of cell‐based therapy to treat ischemic diseases since it is an attractive source for reg...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535497</comments>
            <pubDate>Sat, 24 Dec 2011 02:23:11 +0100</pubDate>
            <guid isPermaLink="false">5535497</guid>        </item>
        <item>
            <title>Suppressor of cytokine signaling 4 (SOCS4): Moderator of ovarian primordial follicle activation</title>
            <link>http://www.medworm.com/index.php?rid=5535496&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22837</link>
            <description>This study demonstrates that the cytokine Leukemia Inhibitory Factor (LIF) activates the Janus Kinase 1/Signal Transducers and Activators of Transcription 3 (JAK1/STAT3) signaling pathway in pre‐granulosa cells and positively regulates primordial follicle activation. Negative regulation of the JAK/STAT pathway is controlled by the suppressor of cytokine signaling 4 (SOCS4) protein, which target members of negative feedback loops, Cardiotrophin like Cytokine (CLC), Poly (rC) Binding Protein 1 (PCBP1), and Cytosolic Malate Dehydrogenase (MDH1) to suppress follicle growth and development. J. Cell. Physiol. 227: 1188–1198, 2012. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535496</comments>
            <pubDate>Sat, 24 Dec 2011 02:23:00 +0100</pubDate>
            <guid isPermaLink="false">5535496</guid>        </item>
        <item>
            <title>Differential response of nucleus pulposus intervertebral disc cells to high salt, sorbitol, and urea</title>
            <link>http://www.medworm.com/index.php?rid=5535495&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22840</link>
            <description>AbstractNucleus pulposus intervertebral disc cells are routinely confronted with high osmolality in their microenvironment and respond to this stress in vitro by regulating cell cycle progression and by activating a DNA repair machinery in order to counteract its genotoxic effect. In the present study, we attempted to identify the origin of this osmo‐regulatory response, by using an ionic NaCl/KCl solution, the compatible osmolyte sorbitol, and the readily permeant urea. High salt and sorbitol were found to activate similar molecular pathways, including the p38 MAPK and the p53‐p21WAF1‐pRb axis, that were not stimulated by high urea. On the other hand, only high urea led to the phosphorylation of ERKs and JNKs. Furthermore, salt‐ and sorbitol‐treated cells were able to phosphoryl...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535495</comments>
            <pubDate>Sat, 24 Dec 2011 02:22:59 +0100</pubDate>
            <guid isPermaLink="false">5535495</guid>        </item>
        <item>
            <title>Stromal cell‐derived factor‐1/CXC receptor 4 and β1 integrin interaction regulates urokinase‐type plasminogen activator expression in human colorectal cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5535494&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22831</link>
            <description>AbstractThe stromal cell‐derived factor‐1 (SDF‐1)/CXC receptor 4 (CXCR4) axis has been shown to play a role in colorectal cancer progression. In addition, the protease urokinase‐type plasminogen activator (uPA) is an important factor in tumor cell invasion and metastasis. However, the mechanism by which SDF‐1 mediates uPA expression in human colorectal cancer cells remains unknown. We investigated the molecular mechanism governing the interaction between SDF‐1 stimulation and uPA expression in three human colon cancer cell lines (DLD‐1, SW48, and COLO 205). We found that SDF‐1 stimulation led to an increase in the expression and secretion of uPA in these cells. Experiments involving specific inhibitors and small interfering RNA demonstrated that the activation of p38 mitoge...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535494</comments>
            <pubDate>Sat, 24 Dec 2011 02:22:50 +0100</pubDate>
            <guid isPermaLink="false">5535494</guid>        </item>
        <item>
            <title>Aryl hydrocarbon receptor‐mediated impairment of chondrogenesis and fracture healing by cigarette smoke and benzo(α)pyrene</title>
            <link>http://www.medworm.com/index.php?rid=5535493&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22819</link>
            <description>AbstractThe clinical literature strongly suggests that bone healing in cigarette smokers is impaired. Since cigarette smoke (CS) contains numerous polycyclic aromatic hydrocarbons (PAHs), and since dioxins impair bone formation in vivo via the Aryl Hydrocarbon Receptor (AHR), we investigated the impact of PAH/AHR signaling on chondrogenesis and on healing in a mouse tibial fracture model. We established that CS activates AHR signaling in fractures by up‐regulating the AHR target gene cytochrome p4501A1 (Cyp1A1). For in vitro studies, we employed the mouse limb bud micromass chondrogenesis model. After confirming that chondrocytes express AHR during differentiation, we treated cells with a prototypical PAH found in CS, benzo(α)pyrene (BaP), or cigarette smoke extract (CSE). Both BaP and ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535493</comments>
            <pubDate>Sat, 24 Dec 2011 02:22:42 +0100</pubDate>
            <guid isPermaLink="false">5535493</guid>        </item>
        <item>
            <title>Enhanced lipid—but not carbohydrate—supported mitochondrial respiration in skeletal muscle of PGC‐1α overexpressing mice</title>
            <link>http://www.medworm.com/index.php?rid=5535492&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22812</link>
            <description>AbstractSkeletal muscle mitochondrial dysfunction has been linked to several disease states as well as the process of aging. A possible factor involved is the peroxisome proliferator‐activated receptor (PPAR) γ co‐activator 1α (PGC‐1α), a major player in the regulation of skeletal muscle mitochondrial metabolism. However, it is currently unknown whether PGC‐1α, besides stimulating mitochondrial proliferation, also affects the functional capacity per mitochondrion. Therefore, we here tested whether PGC‐1α overexpression, besides increasing mitochondrial content, also leads to intrinsic mitochondrial adaptations. Skeletal muscle mitochondria from 10 male, muscle‐specific PGC‐1α overexpressing mice (PGC‐1αTg) and 8 wild‐type (WT) mice were isolated. Equal mitochondria...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535492</comments>
            <pubDate>Sat, 24 Dec 2011 02:22:37 +0100</pubDate>
            <guid isPermaLink="false">5535492</guid>        </item>
        <item>
            <title>Distinct cellular responses induced by saporin and a transferrin–saporin conjugate in two different human glioblastoma cell lines</title>
            <link>http://www.medworm.com/index.php?rid=5535491&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22805</link>
            <description>AbstractGlioblastoma multiforme (GBM) is the most common primary brain tumour in adults, with a median survival of ∼12–18 months post‐diagnosis. GBM usually recurs within 12 months post‐resection, with poor prognosis. Thus, novel therapeutic strategies to target and kill GBM cells are urgently needed. The marked difference of tumour cells with respect to normal brain cells renders glioblastoma a good candidate for selective targeted therapies. Recent experimental strategies focus on over expressed cell surface receptors. Targeted toxins represent a new class of selective molecules composed by a potent protein toxin and a carrier ligand. Targeted toxins approaches against glioblastoma were under investigation in phase I and II clinical trials with several immunotoxins (IT)/ligand to...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535491</comments>
            <pubDate>Sat, 24 Dec 2011 02:22:29 +0100</pubDate>
            <guid isPermaLink="false">5535491</guid>        </item>
        <item>
            <title>Methotrexate chemotherapy reduces osteogenesis but increases adipogenic potential in the bone marrow</title>
            <link>http://www.medworm.com/index.php?rid=5535490&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22807</link>
            <description>AbstractIntensive use of cancer chemotherapy is increasingly linked with long‐term skeletal side effects such as osteopenia, osteoporosis and fractures. However, cellular mechanisms by which chemotherapy affects bone integrity remain unclear. Methotrexate (MTX), used commonly as an anti‐metabolite, is known to cause bone defects. To study the pathophysiology of MTX‐induced bone loss, we examined effects on bone and marrow fat volume, population size and differentiation potential of bone marrow stromal cells (BMSC) in adult rats following chemotherapy for a short‐term (five once‐daily doses at 0.75 mg/kg) or a 6‐week term (5 doses at 0.65 mg/kg + 9 days rest + 1.3 mg/kg twice weekly for 4 weeks). Histological analyses revealed that both acute and chronic MTX treatm...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535490</comments>
            <pubDate>Sat, 24 Dec 2011 02:22:24 +0100</pubDate>
            <guid isPermaLink="false">5535490</guid>        </item>
        <item>
            <title>Development and evaluation of a trehalose‐contained solution formula to preserve hUC‐MSCs at 4°C</title>
            <link>http://www.medworm.com/index.php?rid=5535489&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23066</link>
            <description>In this study, we developed a solution formula that could preserve MSCs at 4°C for up to 3 weeks. In the solution, trehalose is a key ingredient for maintaining survival of MSCs. Among the concentrations investigated, 40 mM trehalose showed the best outcome with the viability maintained more than 92.7 ± 1.5% for 7 days. Cells preserved in the solution formula for 3 weeks still remained about 70% viability, and produced results similar to those of freshly harvested hMSCs in terms of growth kinetics, expression profile of cell surface antigens, and differentiation potential. In summary, storage of MSCs in the medium makes it far easier for transporting the cells from processing units to clinical sites. J. Cell. Physiol. 227: 879–884, 2012. © 2011 Wiley Periodicals, Inc. (Source: J...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535489</comments>
            <pubDate>Sat, 24 Dec 2011 02:22:20 +0100</pubDate>
            <guid isPermaLink="false">5535489</guid>        </item>
        <item>
            <title>Highlights: Volume 227, Number 3</title>
            <link>http://www.medworm.com/index.php?rid=5535488&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23956</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535488</comments>
            <pubDate>Sat, 24 Dec 2011 02:22:19 +0100</pubDate>
            <guid isPermaLink="false">5535488</guid>        </item>
        <item>
            <title>Table of Contents: Volume 227, Number 3</title>
            <link>http://www.medworm.com/index.php?rid=5535487&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23955</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535487</comments>
            <pubDate>Sat, 24 Dec 2011 02:22:17 +0100</pubDate>
            <guid isPermaLink="false">5535487</guid>        </item>
        <item>
            <title>Journal of Cellular Physiology: Volume 227, Number 3, March 2012</title>
            <link>http://www.medworm.com/index.php?rid=5535486&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23954</link>
            <description>AbstractCover: Senescent fibroblasts induced early onset of corneal neovascularization in vivo (n=3). See article in this issue by Zhou et al, pages 1148–1156. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535486</comments>
            <pubDate>Sat, 24 Dec 2011 02:22:16 +0100</pubDate>
            <guid isPermaLink="false">5535486</guid>        </item>
        <item>
            <title>Nuclear IRS‐1 and cancer</title>
            <link>http://www.medworm.com/index.php?rid=5535482&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24019</link>
            <description>AbstractThe family of insulin receptor substrates (IRS) consists of four proteins (IRS‐1 ‐ IRS‐4), which were initially characterized as typical cytosolic adaptor proteins involved in insulin receptor (IR) and insulin‐like growth factor I receptor (IGF‐IR) signaling. The first cloned and characterized member of the IRS family, IRS‐1, has predicted molecular weight of 132 kDa, however, as a result of its extensive serine phosphorylation it separates on a SDS gel as a band of approximately 160‐185 kDa. In addition to its metabolic and growth‐promoting functions, IRS‐1 is also suspected to play a role in malignant transformation. The mechanism by which IRS‐1 supports tumor growth is not fully understood, and the argument that IRS‐1 merely amplifies the signal from the IG...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535482</comments>
            <pubDate>Sat, 24 Dec 2011 02:17:44 +0100</pubDate>
            <guid isPermaLink="false">5535482</guid>        </item>
        <item>
            <title>NALP‐3 inflammasome silencing attenuates ceramide induced transepithelial permeability</title>
            <link>http://www.medworm.com/index.php?rid=5502642&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24026</link>
            <description>AbstractThe hallmark of acute lung injury (ALI) is the influx of proinflammatory cytokines into lung tissue and alveolar permeability that ultimately leads to pulmonary edema. However, the mechanisms involved in inflammatory cytokine production and alveolar permeability are unclear. Recent studies suggest that excessive production of ceramide has clinical relevance as a mediator of pulmonary edema and ALI. Our earlier studies indicate that the activation of inflammasome promotes the processing and secretion of proinflammatory cytokines and causes alveolar permeability in ALI. However, the role of ceramide in inflammasome activation and the underlying mechanism in relation to alveolar permeability is not known. We hypothesized that ceramide activates the inflammasome and causes inflammatory...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5502642</comments>
            <pubDate>Thu, 15 Dec 2011 03:32:32 +0100</pubDate>
            <guid isPermaLink="false">5502642</guid>        </item>
        <item>
            <title>Development and evaluation a trehalose‐contained solution formula to preserve hUC‐MSCs at 4 °C</title>
            <link>http://www.medworm.com/index.php?rid=5502650&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23066</link>
            <description>In this study, we developed a solution formula that could preserve MSCs at 4 °C for up to 3 weeks. In the solution, trehalose is a key ingredient for maintaining survival of MSCs. Among the concentrations investigated, 40mM trehalose showed the best outcome with the viability maintained more than 92.7 ± 1.5% for 7 days. Cells preserved in the solution formula for 3 weeks still remained about 70% viability, and produced results similar to those of freshly harvested hMSCs in terms of growth kinetics, expression profile of cell surface antigens and differentiation potential. In summary, storage of MSCs in the medium makes it far easier for transporting the cells from processing units to clinical sites. J. Cell. Physiol. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physio...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5502650</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5502650</guid>        </item>
        <item>
            <title>The role of COX‐2/PGE2 in gossypol‐induced apoptosis of colorectal carcinoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5502649&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23067</link>
            <description>AbstractOur previous study showed that gossypol (GOS) exhibits potent cytotoxic effects via apoptosis induction against human colorectal carcinoma cells; however the role of cyclooxygenase (COX)‐2/prostaglandin (PG)E2 on GOS‐induced apoptosis is still unknown. In the present study, 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) addition significantly inhibited GOS‐induced apoptosis in human colorectal carcinoma HT‐29 cells in accordance with inducing COX‐2 protein/PGE2 production. TPA inhibition of GOS‐induced apoptosis was blocked by adding protein kinase (PK)C inhibitors including staurosporine (ST), GF109203X (GF), and H7, characterized by the occurrence of cleaved caspase 3 proteins and a decrease in COX‐2 protein/PGE2 production in HT‐29 cells. The addition of ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5502649</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5502649</guid>        </item>
        <item>
            <title>Bone morphogenetic protein receptor type Ia localization causes increased BMP2 signaling in mice exhibiting increased peak bone mass phenotype</title>
            <link>http://www.medworm.com/index.php?rid=5502648&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23028</link>
            <description>This study suggests for the first time a regulatory mechanism of BMPRIa signaling at the plasma membrane of BMSCs that 1) associated with genetic differences in the distal Chromosome 1 segment carried by the B6.C3H‐1‐12 congenic and 2) contributes to increase BMD of the B6.C3H‐1‐12 compared to the C57BL/6J control mice. J. Cell. Physiol. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5502648</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5502648</guid>        </item>
        <item>
            <title>Artichoke polyphenols induce apoptosis and decrease the invasive potential of the human breast cancer cell line MDA‐MB231</title>
            <link>http://www.medworm.com/index.php?rid=5502647&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24029</link>
            <description>AbstractThe human breast cancer cell line, oestrogen receptor negative, MDA‐MB231, was used to evaluate the antitumor effect of polyphenolic extracts from the edible part of artichokes (AEs). Treatment of cancer cells reduced cell viability and inhibited cell growth in a dose‐dependent manner. Importantly, AEs did not have any effect on normal breast epithelial cell line, MCF10A. Chlorogenic acid (ChA), the most representative component of the polyphenolic fraction of artichoke, had no prominent effects on the cell death rate of MDA‐MB231 cells. The addition of AEs to the cells, rather than ChA, triggered apoptosis via a mitochondrial and a death‐receptor pathway, as shown by the activation of caspase‐9 and caspase‐8, respectively. Furthermore, an increase of the Bax:Bcl2 rat...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5502647</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5502647</guid>        </item>
        <item>
            <title>Matrine modulates HSC70 levels and rescues ΔF508‐CFTR</title>
            <link>http://www.medworm.com/index.php?rid=5502646&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24028</link>
            <description>In this report we show that the Matrine, a quinolizidine alkaloid, downregulates the expression of the molecular chaperone HSC70 and increases the protein levels of ΔF508‐CFTR in human alveolar basal epithelial cells (A549 cell line), stably transfected with a ΔF508‐CFTR‐expressing construct. Moreover, Matrine induced ΔF508‐CFTR release from endoplasmic reticulum to cell cytosol and its localization on the cell membrane. Interestingly, downregulation of HSC70 resulted in increased levels of ΔF508‐CFTR complexes with the co‐chaperone BAG3, that in addition appeared to co‐localize with the mutated protein on the cell surface. These results shed new light on ΔF508‐CFTR interactions with proteins of the chaperones/co‐chaperones system and could be useful in strategies fo...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5502646</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5502646</guid>        </item>
        <item>
            <title>MAD2 depletion triggers premature cellular senescence in human primary fibroblasts by activating a P53 pathway preventing aneuploid cells propagation</title>
            <link>http://www.medworm.com/index.php?rid=5502645&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24030</link>
            <description>AbstractThe Spindle Assembly Checkpoint (SAC) is a cellular surveillance mechanism that ensures faithful chromosome segregation during mitosis and its failure can result in aneuploidy. Previously, it was suggested that reduction of the MAD2 gene, encoding a major component of the SAC, induced aneuploidy in human tumor cells. However, tumor cell lines contain multiple mutations that might affect or exacerbate the cellular response to Mad2 depletion. Thus, the scenario resulting by Mad2 depletion in primary human cells could be different and more complex that the one depicted so far. We used primary human fibroblasts (IMR90) and epithelial breast cells (MCF10A) to gain further insight on the effects of genomic instability caused by transient Mad2 depletion. To this aim we depleted Mad2 by RN...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5502645</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5502645</guid>        </item>
        <item>
            <title>Identity and ranking of colonic mesenchymal stromal cells</title>
            <link>http://www.medworm.com/index.php?rid=5502644&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24027</link>
            <description>AbstractAlthough ongoing clinical trials utilize systemic administration of bone‐marrow mesenchymal stromal cells (BM‐MSCs) in Crohn's disease (CD), nothing is known about the presence and the function of MSCs in the normal human bowel. MSCs are bone marrow multipotent cells supporting haematopoiesis with the potential to differentiate into multiple skeletal phenotypes. A recently identified new marker, CD146, allowing to prospectively isolate MSCs from bone marrow, renders also possible their identification in different tissues. In order to elucidate the presence and functional role of MSCs in human bowel we analyzed normal adult colon sections and isolated MSCs from them. In colon (C) sections, resident MSCs form a net enveloping crypts in lamina propria, coinciding with structural m...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5502644</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5502644</guid>        </item>
        <item>
            <title>Critical choices for modeling breast cancer in transgenic mouse models</title>
            <link>http://www.medworm.com/index.php?rid=5502643&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24031</link>
            <description>AbstractModeling breast cancer in the mouse has helped to better define the heterogeneity of human breast cancer. In the recent past, it has become evident that some limitations have restricted the potential benefits that can be achieved with this approach. In this review, we highlight some key points that should be taken into account when the mouse is used, with special emphasis on transgenic models. J. Cell. Physiol. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5502643</comments>
            <pubDate>Wed, 14 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5502643</guid>        </item>
        <item>
            <title>Retraction: Novel approaches for gene‐specific interference via manipulating actions of microRNAs: Examination on the pacemaker channel genes HCN2 and HCN4</title>
            <link>http://www.medworm.com/index.php?rid=5448457&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23060</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5448457</comments>
            <pubDate>Sun, 27 Nov 2011 03:14:41 +0100</pubDate>
            <guid isPermaLink="false">5448457</guid>        </item>
        <item>
            <title>Retraction: Transcriptional activation by stimulating protein 1 and post‐transcriptional repression by muscle‐specific microRNAs of IKs‐encoding genes and potential implications in regional heterogeneity of their expressions</title>
            <link>http://www.medworm.com/index.php?rid=5448456&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23049</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5448456</comments>
            <pubDate>Sun, 27 Nov 2011 03:14:40 +0100</pubDate>
            <guid isPermaLink="false">5448456</guid>        </item>
        <item>
            <title>Retraction: Overexpression HERG K+ channel gene mediates cell‐growth signals on activation of oncoproteins SP1 and NF‐κB and inactivation of tumor suppressor Nkx3.1</title>
            <link>http://www.medworm.com/index.php?rid=5448455&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23050</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5448455</comments>
            <pubDate>Sun, 27 Nov 2011 03:14:38 +0100</pubDate>
            <guid isPermaLink="false">5448455</guid>        </item>
        <item>
            <title>Highlights: Volume 227, Number 2</title>
            <link>http://www.medworm.com/index.php?rid=5448454&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23953</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5448454</comments>
            <pubDate>Sun, 27 Nov 2011 03:13:40 +0100</pubDate>
            <guid isPermaLink="false">5448454</guid>        </item>
        <item>
            <title>Table of Contents: Volume 227, Number 2</title>
            <link>http://www.medworm.com/index.php?rid=5448453&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23952</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5448453</comments>
            <pubDate>Sun, 27 Nov 2011 03:13:39 +0100</pubDate>
            <guid isPermaLink="false">5448453</guid>        </item>
        <item>
            <title>Journal of Cellular Physiology: Volume 227, Number 2, February 2012</title>
            <link>http://www.medworm.com/index.php?rid=5448452&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23951</link>
            <description>AbstractCover: The cover shows transcriptional control of trans‐acting RNA‐Binding Protein in undifferentiated ESC. See mini‐review in this issue by Cassar and Stanford, pages 439–449. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5448452</comments>
            <pubDate>Sun, 27 Nov 2011 03:13:38 +0100</pubDate>
            <guid isPermaLink="false">5448452</guid>        </item>
        <item>
            <title>miR‐520c and miR‐373 upregulate MMP9 expression by targeting mTOR and SIRT1, and activate the Ras/Raf/MEK/Erk signaling pathway and NF‐κB factor in human fibrosarcoma cells</title>
            <link>http://www.medworm.com/index.php?rid=5438945&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22993</link>
            <description>In conclusion, miR‐520c and miR‐373 increased the expression of MMP9 by directly targeting the 3′‐UTRs of mRNAs of mTOR and SIRT1 and suppressing their translation; resulting in activation of the Ras/Raf/MEK/Erk signaling pathway and NF‐κB; and, finally, increasing the mRNA, protein, and activity of MMP9 and enhancing cell migration and cell growth in 3D type I collagen gels. J. Cell. Physiol. 227: 867–876, 2012. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438945</comments>
            <pubDate>Thu, 24 Nov 2011 01:42:10 +0100</pubDate>
            <guid isPermaLink="false">5438945</guid>        </item>
        <item>
            <title>Human mesenchymal stem cells seeded on extracellular matrix‐scaffold: Viability and osteogenic potential</title>
            <link>http://www.medworm.com/index.php?rid=5438944&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22983</link>
            <description>AbstractThe development and the optimization of novel culture systems of mesenchymal osteoprogenitors are some of the most important challenges in the field of bone tissue engineering (TE). A new combination between cells and extracellular matrix (ECM)‐scaffold, containing ECM has here been analyzed. As source for osteoprogenitors, mesenchymal stem cells obtained from human umbilical cord Wharton's Jelly (hWJMSCs), were used. As ECM‐scaffold, a powder form of isolated and purified porcine urinary bladder matrix (pUBM), was employed. The goals of the current work were: (1) the characterization of the in vitro hWJMSCs behavior, in terms of viability, proliferation, and adhesion to ECM‐scaffold; (2) the effectiveness of ECM‐scaffold to induce/modulate the osteoblastic differentiation;...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438944</comments>
            <pubDate>Thu, 24 Nov 2011 01:42:09 +0100</pubDate>
            <guid isPermaLink="false">5438944</guid>        </item>
        <item>
            <title>MiR‐133a regulates collagen 1A1: Potential role of miR‐133a in myocardial fibrosis in angiotensin II‐dependent hypertension</title>
            <link>http://www.medworm.com/index.php?rid=5438943&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22939</link>
            <description>AbstractMicroRNAs play an important role in myocardial diseases. MiR‐133a regulates cardiac hypertrophy, while miR‐29b is involved in cardiac fibrosis. The aim of this study was to evaluate whether miR‐133a and miR‐29b play a role in myocardial fibrosis caused by Angiotensin II (Ang II)‐dependent hypertension. Sprague–Dawley rats were treated for 4 weeks with Ang II (200 ng/kg/min) or Ang II + irbesartan (50 mg/kg/day in drinking water), or saline by osmotic minipumps. At the end of the experimental period, cardiac miR‐133a and miR‐29b expression was measured by real‐time PCR, and myocardial fibrosis was evaluated by morphometric analysis. A computer‐based prediction algorithm led to the identification of collagen 1a1 (Col1A1) as a putative target of miR‐133a....</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438943</comments>
            <pubDate>Thu, 24 Nov 2011 01:42:08 +0100</pubDate>
            <guid isPermaLink="false">5438943</guid>        </item>
        <item>
            <title>Wnt/β‐catenin signaling pathway and thioredoxin‐interacting protein (TXNIP) mediate the “glucose sensor” mechanism in metastatic breast cancer‐derived cells MDA‐MB‐231</title>
            <link>http://www.medworm.com/index.php?rid=5438942&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22757</link>
            <description>In this study we investigated the effect of glucose on GSK3β and β‐catenin expression and the involvement of the N‐linked glycosylation and hexosamine pathways in the Wnt canonical pathway in response to in vitro conditions resembling normoglycemia (5 mmol) and hyperglycemia (20 mmol) in the metastatic breast cancer‐derived cell line MDA‐MB‐231. We also investigated the relationship between this circuitry and the thioredoxin‐interacting protein (TXNIP) regulation that seems to be related. MDA‐MB‐231 cells were grown either in 5 or 20 mM glucose chronically prior to plating. For glucose shift (5/20), cells were plated in 5 mM glucose and shifted to 20 mM at time 0. Both protein and mRNA levels for GSK3β but only the protein expression for β‐catenin, were incr...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438942</comments>
            <pubDate>Thu, 24 Nov 2011 01:41:36 +0100</pubDate>
            <guid isPermaLink="false">5438942</guid>        </item>
        <item>
            <title>Hyperglycemia induces apoptosis via CB1 activation through the decrease of FAAH 1 in retianl pigment epithelial cells</title>
            <link>http://www.medworm.com/index.php?rid=5438941&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22756</link>
            <description>In conclusion, HG‐induced apoptosis in ARPE‐19 cells by inducing CB1R expression through the downregulation of FAAH 1 expression. Our results provide evidence that CB1R blockade through the recovery of FAAH 1 expression may be a potential anti‐diabetic therapy for the treatment of diabetic retinopathy. J. Cell. Physiol. 227: 569–577, 2012. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438941</comments>
            <pubDate>Thu, 24 Nov 2011 01:41:35 +0100</pubDate>
            <guid isPermaLink="false">5438941</guid>        </item>
        <item>
            <title>Functional regulation of HIF‐1α under normoxia—is there more than post‐translational regulation?</title>
            <link>http://www.medworm.com/index.php?rid=5438940&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22798</link>
            <description>AbstractThe hypoxia‐inducible factor‐1 (HIF‐1) is an oxygen‐regulated transcriptional activator playing a pivotal role in mammalian physiology and disease pathogenesis, e.g., HIF‐1 is indispensable in a broad range of developmental stages in different tumors. Its post‐translational regulation via PHDs under the influence of hypoxia is widely investigated and accepted. Different non‐hypoxic stimuli such as lipopolysaccharides (LPS), thrombin, and angiotensin II (Ang II), have been proven to enhance HIF‐1 levels through activation of regulative mechanisms distinct from protein stabilization. Some of these stimuli specifically regulate HIF‐1α at the transcriptional, post‐transcriptional, or translational level, whereas others additionally influence post‐translational mo...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438940</comments>
            <pubDate>Thu, 24 Nov 2011 01:41:29 +0100</pubDate>
            <guid isPermaLink="false">5438940</guid>        </item>
        <item>
            <title>The switch from pRb/p105 to Rb2/p130 in DNA damage and cellular senescence</title>
            <link>http://www.medworm.com/index.php?rid=5438939&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22786</link>
            <description>AbstractCellular senescence is a response to genotoxic stress that results in an irreversible cell cycle arrest. Activation of this pathway relies on the activity of the retinoblastoma proteins and proteins of the DNA damage response cascade. Here, we discuss the functional relevance of the switch from pRb/p105 to Rb2/p130 that becomes apparent when cells enter senescent arrest. J. Cell. Physiol. 227: 508–513, 2012. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438939</comments>
            <pubDate>Thu, 24 Nov 2011 01:41:28 +0100</pubDate>
            <guid isPermaLink="false">5438939</guid>        </item>
        <item>
            <title>Orthopedic gene therapy—lost in translation?</title>
            <link>http://www.medworm.com/index.php?rid=5438938&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23031</link>
            <description>AbstractOrthopedic gene therapy has been the topic of considerable research for two decades. The preclinical data are impressive and many orthopedic conditions are well suited to genetic therapies. But there have been few clinical trials and no FDA‐approved product exists. This paper examines why this is so. The reasons are multifactorial. Clinical translation is expensive and difficult to fund by traditional academic routes. Because gene therapy is viewed as unsafe and risky, it does not attract major funding from the pharmaceutical industry. Start‐up companies are burdened by the complex intellectual property environment and difficulties in dealing with the technology transfer offices of major universities. Successful translation requires close interactions between scientists, clinic...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438938</comments>
            <pubDate>Thu, 24 Nov 2011 01:41:16 +0100</pubDate>
            <guid isPermaLink="false">5438938</guid>        </item>
        <item>
            <title>Bone production by human maxillary sinus mucosa cells</title>
            <link>http://www.medworm.com/index.php?rid=5438919&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24022</link>
            <description>AbstractThe Schneider membrane is the mucosa that covers the inner part of the maxillary sinus cavities. The free surface is a ciliated pseudostratified epithelium, while the deeper portion is a highly vascularised connective tissue. The stromal fraction, bordering the bony wall of the sinus, after tooth loss can exhibit increased osteoclastic activity resulting in resorption of the bone in the posterior maxilla.Goal of our study was to isolate and characterize mesenchymal progenitors in the Schneider's membrane connective net and to evaluate their self ability to differentiate towards osteoblastic lineage, in absence of osteoinductive factors and osteoconductive biomaterials of support. This should indicate that maxillary sinus membrane represents an useful an approachable source of MSCs ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438919</comments>
            <pubDate>Thu, 24 Nov 2011 01:36:12 +0100</pubDate>
            <guid isPermaLink="false">5438919</guid>        </item>
        <item>
            <title>Phamaco‐metabolomics: an emerging “omics” tool for the personalization of anticancer treatments and identification of new valuable therapeutic targets</title>
            <link>http://www.medworm.com/index.php?rid=5438937&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24003</link>
            <description>AbstractIn the post‐genomics era, metabolomics represents a new “omics” approach that in the last decade has received increased attention in the field of oncology. Metabolomics is based on the holistic study of the metabolic profile that characterizes a specific phenotype in a biological system. The metabolic profile provides a readout of the metabolic state of an individual that cannot be obtained directly from DNA genotyping, gene expression or proteomic profiling analyses. The translational value of metabonomics in the oncology field has been demonstrated by the identification of diagnostic and prognostic biomarkers. The so‐called pharmaco‐metabolomic approach that is currently emerging aims to identify the individual metabolomic characteristics able to predict drug effectiven...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438937</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438937</guid>        </item>
        <item>
            <title>Alveolar macrophage dynamics in murine lung regeneration</title>
            <link>http://www.medworm.com/index.php?rid=5438936&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24009</link>
            <description>AbstractIn most mammalian species, the removal of one lung results in dramatic compensatory growth of the remaining lung. To investigate the contribution of alveolar macrophages (AM) to murine post‐pneumonectomy lung growth, we studied bronchoalveolar lavage (BAL)‐derived AM on 3, 7, 14 and 21 days after left pneumonectomy. BAL demonstrated a 3.0‐fold increase in AM (CD45+, CD11b‐, CD11c+, F4/80+, Gr‐1‐) by 14 days after pneumonectomy. Cell cycle flow cytometry of the BAL‐derived cells demonstrated an increase in S + G2 phase cells on days 3 (11.3+ 2.7%) and 7 (12.1 + 1.8%) after pneumonectomy. Correspondingly, AM demonstrated increased expression of VEGFR1 and MHC class II between days 3 and 14 after pneumonectomy. To investigate the potential contribution of periphe...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438936</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438936</guid>        </item>
        <item>
            <title>Crosstalk between adenosine A1 and β1‐adrenergic receptors regulates translocation of PKCε in isolated rat cardiomyocytes</title>
            <link>http://www.medworm.com/index.php?rid=5438935&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24008</link>
            <description>AbstractAdenosine A1 receptor (A1R)‐induced translocation of PKCε to transverse (t) tubular membranes in isolated rat cardiomyocytes is associated with a reduction in β1‐adrenergic‐stimulated contractile function. The PKCε‐mediated activation of protein kinase D (PKD) by endothelin‐1 is inhibited by β1‐adrenergic stimulated protein kinase A (PKA) suggesting a similar mechanism of A1R signal transduction modulation by adrenergic agonists may exist in the heart. We have investigated the influence of β1‐adrenergic stimulation on PKCε translocation elicited by A1R. Immunofluorescence imaging and Western blotting with PKCε and β‐COP antibodies were used to quantify the co‐localization of PKCε and t‐tubular structures in isolated rat cardiomyocytes. The A1R agonist C...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438935</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438935</guid>        </item>
        <item>
            <title>Unsaturated fatty acids induce mesenchymal stem cells to increase secretion of angiogenic mediators</title>
            <link>http://www.medworm.com/index.php?rid=5438934&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24013</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438934</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438934</guid>        </item>
        <item>
            <title>The seventh ring: exploring TRAF7 functions</title>
            <link>http://www.medworm.com/index.php?rid=5438933&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24011</link>
            <description>AbstractTumor necrosis factor receptor associated factors (TRAFs) have been discovered and characterized by their capacity to link Tumor Necrosis Factor Receptors (TNFR)‐family proteins to signaling pathways that transduce the cellular effects mediated by TNF‐family ligands. There are seven known mammalian TRAF proteins (TRAF1‐7), that share a domain organization made of a modular structure, characteristic of adaptor proteins whose function is to link structurally dissimilar factors. Functionally, TRAF proteins mediate the assembly of cytoplasmic signal transducers and regulatory molecules downstream of receptors complexes. Despite the similarities in the signaling pathways activated by the different TRAF proteins, each appears to play distinct physiological roles. TRAF7 is the last ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438933</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438933</guid>        </item>
        <item>
            <title>The protective role of peroxisome proliferator‐activated receptor γ coactivator‐1α in hyperthyroid cardiac hypertrophy</title>
            <link>http://www.medworm.com/index.php?rid=5438932&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24015</link>
            <description>AbstractHeart failure is a major cause of death throughout the world. Hyperthyroidism has been shown to induce cardiac hypertrophy, which is a contributing factor to heart failure. However, the mechanism underling effect of thyroid hormone is not completely clear. The present study investigates the role of peroxisome proliferator‐activated receptor (PPAR) γ coactivator‐1α (PGC‐1α) in cardiac hypertrophy induced by Triiodothyronine (T3). We investigated PGC‐1α mRNA expression in rat hearts exposed to T3 in vivo and ex vivo. Surprisingly, we found that the extended periods of T3 treatment led to an increase in PGC‐1α expression compared to shorter treatment times, which resulted in a reduction of PGC‐1α expression. Mechanistic studies showed that suppression of PGC‐1α by...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438932</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438932</guid>        </item>
        <item>
            <title>Differential mesengenic potential and expression of stem cell fate modulators in mesenchymal stromal cells from human term placenta and bone marrow</title>
            <link>http://www.medworm.com/index.php?rid=5438931&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24014</link>
            <description>In this study, we have characterized ex vivo expanded MSCs from the human amniotic (hAMSCs) and chorionic (hCMSCs) membranes of human full term placentas and adult bone marrow (hBMSCs). Our results show that hAMSCs, hCMSCs and hBMSCs express typical mesenchymal (CD73, CD90, CD105, CD44, CD146, CD166) and pluripotent (Oct‐4, Sox2, Nanog, Lin28 and Klf4) markers but not hematopoietic markers (CD45, CD34). Ex vivo expanded hAMSCs were found to be of fetal origin, while hCMSCs cultures contained only maternal cells. Cell proliferation was significantly higher in hCMSCs, compared to hAMSCs and hBMSCs. Integrin profiling revealed marked differences in the expression of α − subunits between the three cell sources. Cadherin receptors were consistently expressed on a subset of progenitors ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438931</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438931</guid>        </item>
        <item>
            <title>Vitamin C treatment promotes mesenchymal stem cell sheet formation and tissue regeneration by elevating telomerase activity</title>
            <link>http://www.medworm.com/index.php?rid=5438930&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24012</link>
            <description>In this study, we found that vitamin C (Vc) was capable of inducing telomerase activity in periodontal ligament stem cells (PDLSCs), leading to the up‐regulated expression of extracellular matrix type I collagen, fibronectin, and integrin β1, stem cell markers Oct4, Sox2, and Nanog as well as osteogenic markers RUNX2, ALP, OCN. Under Vc treatment, PDLSCs can form cell sheet structures because of increased cell matrix production. Interestingly, PDLSC sheets demonstrated a significant improvement in tissue regeneration compared with untreated control dissociated PDLSCs and offered an effective treatment for periodontal defects in a swine model. In addition, bone marrow mesenchymal stem cell sheets and umbilical cord mesenchymal stem cell sheets were also well constructed using this method...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438930</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438930</guid>        </item>
        <item>
            <title>New insights in endometrial carcinogenesis</title>
            <link>http://www.medworm.com/index.php?rid=5438929&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24016</link>
            <description>AbstractEndometrial carcinoma is the most common cancer of the female genital tract in Europe and in the United States. Despite advances in defining the biology of endometrial carcinomas, there has been poor progress in determining markers that distinguish preinvasive endometrial proliferations.The aim of this review is to highlight the most recent studies regarding the molecular markers involved in endometrial adenocarcinoma pathogenesis and carcinogenesis. We focus on studies that describe markers with potential to progress from endometrial hyperplasia to invasive disease. J. Cell. Physiol. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438929</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438929</guid>        </item>
        <item>
            <title>Human myxomatous mitral valve prolapse: Role of bone morphogenetic protein 4 in valvular interstitial cell activation</title>
            <link>http://www.medworm.com/index.php?rid=5438928&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22999</link>
            <description>AbstractMyxomatous Mitral valve prolapse (MVP) is the most common cardiac valvular abnormality in industrialized countries and a leading cause of mitral valve surgery for isolated mitral regurgitation. The key role of valvular interstitial cells (VICs) during mitral valve development and homeostasis has been recently suggested, however little is known about the molecular pathways leading to MVP. We aim to characterize Bone Morphogenetic Protein 4 (BMP4) as a cellular regulator of mitral valvular interstitial cell activation towards a pathologic synthetic phenotype and to analyze the cellular phenotypic changes and extracellular matrix (ECM) reorganization associated with the development of myxomatous mitral valve prolapse. Microarray analysis showed significant up regulation of BMP4‐medi...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438928</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438928</guid>        </item>
        <item>
            <title>Proteotoxic stress of cancer: implication of the heat‐shock response in oncogenesis</title>
            <link>http://www.medworm.com/index.php?rid=5438927&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24017</link>
            <description>AbstractOrganisms frequently encounter a wide variety of proteotoxic stressors. The heat‐shock response, an ancient cytoprotective mechanism, has evolved to augment organismal survival and longevity in the face of proteotoxic stress from without and within. These broadly recognized beneficial effects, ironically, contrast sharply with its emerging role as a culprit in the pathogenesis of cancers. Here, we present an overview of the normal biology of the heat‐shock response and highlight its implications in oncogenic processes, including the proteotoxic stress phenotype of cancer; the function of this stress response in helping cancer survive and adapt to proteotoxic stress; and perturbation of proteome homeostasis in cancer as a potential therapeutic avenue. J. Cell. Physiol. © 2011 W...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438927</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438927</guid>        </item>
        <item>
            <title>Evidence of Vitamin D and interferon‐β cross‐talk in human osteoblasts with 1α,25‐dihydroxyvitamin D3 being dominant over interferon‐β in stimulating mineralization</title>
            <link>http://www.medworm.com/index.php?rid=5438926&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24020</link>
            <description>In conclusion, the current study demonstrates a cross‐talk between 1,25D3 and IFNβ in osteoblast differentiation and bone formation/mineralization. The interaction is complex and depends on the process but importantly, 1,25D3 stimulation of mineralization is dominant over the inhibitory effect of IFNβ. These observations are of potential clinical relevance considering the impact of the immune system on bone metabolism in conditions such as rheumatoid arthritis. J. Cell. Physiol. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438926</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438926</guid>        </item>
        <item>
            <title>Homogentisate 1,2 dioxygenase is expressed in human osteoarticular cells: Implications in alkaptonuria</title>
            <link>http://www.medworm.com/index.php?rid=5438925&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24018</link>
            <description>AbstractAlkaptonuria (AKU) results from defective homogentisate1,2‐dioxygenase (HGD), causing degenerative arthropathy. The deposition of ochronotic pigment in joints is so far attributed to homogentisic acid produced by the liver, circulating in the blood and accumulating locally. Human normal and AKU osteoarticular cells were tested for HGD gene expression by RT‐PCR, mono‐ and 2D‐western blotting. HGD gene expression was revealed in chondrocytes, synoviocytes, osteoblasts. Furthermore, HGD expression was confirmed by western blotting, that also revealed the presence of five enzymatic molecular species. Our findings indicate that AKU osteoarticular cells produce the ochronotic pigment in loco and this may strongly contribute to induction of ochronotic arthropathy. J. Cell. Physiol...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438925</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438925</guid>        </item>
        <item>
            <title>Apert syndrome mutant FGFR2 and its soluble form reciprocally alter osteogenesis of primary calvarial osteoblasts</title>
            <link>http://www.medworm.com/index.php?rid=5438924&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24021</link>
            <description>In this study, we characterized the effects of one of the mutations (S252W) using primary calvarial osteoblasts derived from transgenic mice, Ap‐Tg and sAp‐Tg, that expressed an Apert‐type mutant FGFR2 (FGFR2IIIc‐S252W; FGFR2IIIc‐Ap), and the soluble form (extracellular domain only) of the mutant FGFR2 (sFGFR2IIIc‐Ap), respectively. Compared to WT‐derived osteoblasts, osteoblasts from Ap‐Tg mouse showed a higher proliferative activity and enhanced differentiation, while those from sAp‐Tg mouse exhibited reduced potential for proliferation and osteogenic differentiation. When transplanted with β‐tricalcium phosphate (β‐TCP) granules into immunodeficient mice, Ap‐Tg‐derived osteoblasts showed a higher bone forming capacity, whereas sAp‐Tg‐derived osteoblasts w...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438924</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438924</guid>        </item>
        <item>
            <title>Depletion of GRIM‐19 accelerates hepatocellular carcinoma invasion via inducing EMT and loss of contact inhibition</title>
            <link>http://www.medworm.com/index.php?rid=5438923&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24025</link>
            <description>Conclusion: Our observations demonstrate a novel mechanistic insight into a critical role of GRIM‐19 in HCC invasive potential. J. Cell. Physiol. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438923</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438923</guid>        </item>
        <item>
            <title>TGF β‐1 administration during ex‐vivo expansion of human articular chondrocytes in a serum‐free medium redirects the cell phenotype toward hypertrophy</title>
            <link>http://www.medworm.com/index.php?rid=5438922&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24024</link>
            <description>AbstractCell‐based cartilage resurfacing requires ex‐vivo expansion of autologous articular chondrocytes. Defined culture conditions minimize expansion‐dependent phenotypic alterations but maintenance of the cells' differentiation potential must be carefully assessed. TGF ß‐1 positively regulates the expression of several cartilage proteins, but its therapeutic application in damaged cartilage is controversial. Thus we evaluated the phenotypic outcomes of cultured human articular chondrocytes exposed to TGF β‐1 during monolayer expansion in a serum‐free medium. After 5 doublings cells were transferred to micromass cultures to assess their chondrogenic differentiation, or replated in osteogenic medium. Immunocytostainings of micromasses of TGF‐expanded cells showed loss of a...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438922</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438922</guid>        </item>
        <item>
            <title>Potential Role of Prolactin in Antipsychotic‐Mediated Association of Schizophrenia and Type 2 Diabetes</title>
            <link>http://www.medworm.com/index.php?rid=5438920&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24023</link>
            <description>AbstractIt remains unclear why atypical antipsychotics confer a risk for hyperglycemia compared to typical antipsychotics. Atypical antipsychotics antagonize dopamine receptors‐2 (D2) and serotonin (5‐HT) receptors‐2, while typical antipsychotics antagonize only D2 receptors.We aimed at elucidating the mechanistic differences between the role of typical and atypical antipsychotics on prolactin levels and glucose regulation.A Medline search was conducted during 2010 using the search terms type 2 diabetes (T2D), typical/atypical antipsychotics, schizophrenia, prolactin, and serotonin. We discuss the effect of typical and atypical antipsychotics on prolactin levels and glucose regulation.Given that prolactin is under negative control by dopamine and positive control by serotonin, typica...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438920</comments>
            <pubDate>Mon, 21 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438920</guid>        </item>
        <item>
            <title>Highlights: Volume 227, Number 1</title>
            <link>http://www.medworm.com/index.php?rid=5378353&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23950</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378353</comments>
            <pubDate>Sat, 05 Nov 2011 22:12:40 +0100</pubDate>
            <guid isPermaLink="false">5378353</guid>        </item>
        <item>
            <title>Table of Contents: Volume 227, Number 1</title>
            <link>http://www.medworm.com/index.php?rid=5378352&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23949</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378352</comments>
            <pubDate>Sat, 05 Nov 2011 22:12:38 +0100</pubDate>
            <guid isPermaLink="false">5378352</guid>        </item>
        <item>
            <title>Journal of Cellular Physiology: Volume 227, Number 1, January 2012</title>
            <link>http://www.medworm.com/index.php?rid=5378351&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23948</link>
            <description>AbstractCover: The cover shows a protein‐protein interaction landscape of essential transcription factors in ESC. Please see review article by Mallanna and Rizzino in this issue, pages 27–34. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378351</comments>
            <pubDate>Sat, 05 Nov 2011 22:12:37 +0100</pubDate>
            <guid isPermaLink="false">5378351</guid>        </item>
        <item>
            <title>Extracellular calcium chronically‐induced human osteoblasts effects: Specific modulation of osteocalcin and collagen type XV</title>
            <link>http://www.medworm.com/index.php?rid=5356969&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24001</link>
            <description>In conclusion, our data show a clear phenotypical and functional effect of extracellular Ca2+ on human osteoblasts and support the hypothesis of a direct role of this cation in the bone remodeling processes. J. Cell. Physiol. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5356969</comments>
            <pubDate>Fri, 28 Oct 2011 20:52:33 +0100</pubDate>
            <guid isPermaLink="false">5356969</guid>        </item>
        <item>
            <title>JCV agnoprotein‐induced reduction in CXCL5/LIX secretion by oligodendrocytes is associated with activation of apoptotic signaling in neurons</title>
            <link>http://www.medworm.com/index.php?rid=5356974&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23065</link>
            <description>AbstractAn indispensable role for oligodendrocytes in the protection of axon function and promotion of neuronal survival is strongly supported by the finding of progressive neuron/axon degeneration in human neurological diseases that affect oligodendrocytes. Imaging and pathological studies of the CNS have shown the presence of neuroaxonal injury in progressive multifocal leukoencephalopathy (PML), a demyelinating disease of the CNS, resulting from destruction of oligodendrocytes upon productive replication of the pathogenic neurotropic polyomavirus JC. Here, we examined the extracellular factors involved in communication between oligodendrocytes and neurons. Culturing cortical neurons with conditioned medium (CM) from rat CG4 oligodendrocytic cells that express the JCV agnoprotein showed ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5356974</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5356974</guid>        </item>
        <item>
            <title>MicroRNA‐21 represses human cystathionine gamma‐lyase expression by targeting at specificity protein‐1 in smooth muscle cells</title>
            <link>http://www.medworm.com/index.php?rid=5356973&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24006</link>
            <description>AbstractCystathionine gamma‐lyase (CSE) is the major H2S‐generating enzyme in vascular smooth muscle cells (SMCs). CSE/H2S system contributes to the maintenance of SMC phenotype, and transcript factor specificity protein‐1 (SP1) is a critical regulator of CSE expression during SMC differentiation. The involvements of microRNA‐21 (miR‐21) in cardiovascular pathophysiology have been known, however miR‐21 regulation of CSE and SP1 as well as SMC phenotype are uncertain. Using quantitative real‐time PCR, we demonstrated that the expression of miR‐21 was upregulated in dedifferentiated human aorta SMCs (HASMCs) and injured mouse carotid arteries. To determine the potential roles of miR‐21 in SP1‐mediated CSE gene expression and SMC phenotypic change, we showed that miR‐21 ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5356973</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5356973</guid>        </item>
        <item>
            <title>Ox‐LDL‐induced TGF‐β1 production in human alveolar epithelial cells: involvement of the Ras/ERK/ PLTP pathway</title>
            <link>http://www.medworm.com/index.php?rid=5356972&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24005</link>
            <description>In this study, we investigated whether Ox‐LDL can induce TGF‐β1 protein production, and if so, how it achieves this induction in human alveolar epithelial cells (A549). We show here that Ox‐LDL not only caused a dose‐ and time‐dependent up‐regulation of TGF‐β1 production, but also increased Smad3 phosphorylation, Ras/extracellular signal‐regulated kinase(ERK) activity and phospholipid transfer protein (PLTP) expression in A549 cells. The inhibition of Ras/ERK activity with specific inhibitors significantly suppressed Ox‐LDL‐induced TGF‐β1 production, Smad3 phosphorylation and PLTP expression. Furthermore, treatment of cells with PLTP siRNA suppressed both TGF‐β1 release and Smad3 activation induced by Ox‐LDL, but not the activation of Ras/ERK cascade. Taken ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5356972</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5356972</guid>        </item>
        <item>
            <title>Epigenetics of µ‐opioid receptors: Intersection with HIV‐1 infection of the central nervous system</title>
            <link>http://www.medworm.com/index.php?rid=5356971&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24004</link>
            <description>AbstractThe abuse of intravenous drugs, such as heroin, has become a major public health concern due to the increased risk of HIV‐1 infection. Opioids such as heroin were originally identified and subsequently abused for their analgesic effects. However, many investigations have found additional effects of opioids, including regulation of the immune system. As such, chronic opioid abuse has been shown to promote HIV‐1 pathogenesis and facilitate HIV‐1‐associated neurocognitive dysfunction. Clinical opioids, such as morphine and methadone, as well as illicit opioids, such as heroin, exert their effects primarily through interactions with the µ‐opioid receptor (MOR). However, the mechanisms by which opioids enhance neurocognitive dysfunction through MOR‐mediated signaling pathwa...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5356971</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5356971</guid>        </item>
        <item>
            <title>Challenges and opportunities of metabolomics</title>
            <link>http://www.medworm.com/index.php?rid=5356970&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24002</link>
            <description>AbstractThe metabolome is a data‐rich source of information concerning all the low‐molecular‐weight metabolites in a biofluid, which can indicate early biological changes to the host due to perturbations in metabolic pathways. Major changes can be seen after minor stimuli, which make it a valuable target for analysis. Due to the diverse and sensitive nature of the metabolome, studies must be designed in a manner to maintain consistency, reduce variation between subjects, and optimize information recovery. Technological advancements in experimental design, mouse models and instrumentation have aided in this effort. Metabolomics has the ultimate potential to be valuable in a clinical setting where it could be used for early diagnosis of a disease and as a predictor of treatment respons...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5356970</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5356970</guid>        </item>
        <item>
            <title>Nuclear γ‐tubulin associates with nucleoli and interacts with tumor suppressor protein C53</title>
            <link>http://www.medworm.com/index.php?rid=5344994&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22772</link>
            <description>Abstractγ‐Tubulin is assumed to be a typical cytosolic protein necessary for nucleation of microtubules from microtubule organizing centers. Using immunolocalization and cell fractionation techniques in combination with siRNAi and expression of FLAG‐tagged constructs, we have obtained evidence that γ‐tubulin is also present in nucleoli of mammalian interphase cells of diverse cellular origins. Immunoelectron microscopy has revealed γ‐tubulin localization outside fibrillar centers where transcription of ribosomal DNA takes place. γ‐Tubulin was associated with nucleolar remnants after nuclear envelope breakdown and could be translocated to nucleoli during mitosis. Pretreatment of cells with leptomycin B did not affect the distribution of nuclear γ‐tubulin, making it unlikely...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5344994</comments>
            <pubDate>Mon, 24 Oct 2011 23:41:28 +0100</pubDate>
            <guid isPermaLink="false">5344994</guid>        </item>
        <item>
            <title>MAP kinase mediates silica‐induced fibrotic nodule formation and collagen accumulation in fibroblasts</title>
            <link>http://www.medworm.com/index.php?rid=5344993&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22739</link>
            <description>AbstractIt is well known that silica generates fibrosis around them in animals and human. However, the pathogenesis and mechanism of silica‐induced fibrosis are still poorly understood. Here, we established a new strategy through which the effects of silica on fibrotic nodule formation, key extracellular matrix accumulation, and the mechanism involved were explored. To achieve this, human dermal fibroblasts were directly exposed to silica gel for various durations. Fibrotic nodule formation was evaluated by their microscopic appearance, type‐1 procollagen, and fibronection expression in cell lysate and MMP‐1 and‐3 in conditioned media were analyzed by Western blotting. The results show an easily formation of nodule‐like structures around silica gel in an in vitro‐cultured syste...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5344993</comments>
            <pubDate>Mon, 24 Oct 2011 23:41:23 +0100</pubDate>
            <guid isPermaLink="false">5344993</guid>        </item>
        <item>
            <title>Chromosomal instability in mouse embryonic fibroblasts null for the transcriptional co‐repressor Ski</title>
            <link>http://www.medworm.com/index.php?rid=5344992&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22733</link>
            <description>AbstractSki is a transcriptional regulator that has been considered an oncoprotein given its ability to induce oncogenic transformation in avian model systems. However, studies in mouse and in some human tumor cells have also indicated a tumor suppressor activity for this protein. We found that Ski−/− mouse embryo fibroblasts exhibit high levels of genome instability, namely aneuploidy, consistent with a tumor suppressor function for Ski. Time‐lapse microscopy revealed lagging chromosomes and chromatin/chromosome bridges as the major cause of micronuclei (MN) formation and the subsequent aneuploidy. Although these cells arrested in mitosis after treatment with spindle disrupting drugs and exhibited a delayed metaphase/anaphase transition, spindle assembly checkpoint (SAC) was not suf...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5344992</comments>
            <pubDate>Mon, 24 Oct 2011 23:41:17 +0100</pubDate>
            <guid isPermaLink="false">5344992</guid>        </item>
        <item>
            <title>Protective effects of adiponectin against renal ischemia‐reperfusion injury via prostacyclin‐PPARα‐Heme oxygenase‐1 signaling pathway</title>
            <link>http://www.medworm.com/index.php?rid=5344991&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22726</link>
            <description>In conclusion, our results provide a novel APN mediated prostacyclin‐PPARα‐HO‐1 signaling pathway in protecting renal I/R injury. J. Cell. Physiol. 227: 239–249, 2012. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5344991</comments>
            <pubDate>Mon, 24 Oct 2011 23:41:13 +0100</pubDate>
            <guid isPermaLink="false">5344991</guid>        </item>
        <item>
            <title>Arsenic induced progesterone production in a caspase‐3‐dependent manner and changed redox status in preovulatory granulosa cells</title>
            <link>http://www.medworm.com/index.php?rid=5344990&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22717</link>
            <description>AbstractArsenic contamination is a principal environmental health threat throughout the world. However, little is known about the effect of arsenic on steroidogenesis in granulosa cells (GCs). We found that the treatment of preovulatory GCs with arsenite stimulated progesterone production. A significant increase in serum level of progesterone was observed in female Sprague–Dawley rats following arsenite treatment at a dose of 10 mg/L/rat/day for 7 days. Further experiments demonstrated that arsenite treatment did not change the level of intracellular cyclic AMP (cAMP) or phosphorylated ERK1/2 in preovulatory GCs; however, progesterone production was significantly decreased when cAMP‐dependent protein kinase (PKA) or ERK1/2 pathway was inhibited. This implied that the effect of arseni...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5344990</comments>
            <pubDate>Mon, 24 Oct 2011 23:41:07 +0100</pubDate>
            <guid isPermaLink="false">5344990</guid>        </item>
        <item>
            <title>MicroRNA 21 regulates the proliferation of human adipose tissue‐derived mesenchymal stem cells and high‐fat diet‐induced obesity alters microRNA 21 expression in white adipose tissues</title>
            <link>http://www.medworm.com/index.php?rid=5344989&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22716</link>
            <description>In this study, we determined the expression of miR‐21 in white adipose tissues in a high‐fat diet (HFD)‐induced obesity mouse model to examine the relationship between miR‐21 and obesity and the effect of miR‐21 on hASCs proliferation. Our study showed biphasic changes of miR‐21 expression and a correlation between miR‐21 level and adipocyte number in the epididymal fat of HFD mice. Over‐expression of miR‐21 decreased cell proliferation, whereas inhibiting miR‐21 with 2′‐O‐methyl‐antisense RNA increased it. Over‐expression of miR‐21 decreased both protein and mRNA levels of STAT3, whereas inhibiting miR‐21 with 2′‐O‐methyl‐antisense RNA increased these levels. The activity of a luciferase construct containing the miR‐21 target site from the STAT3...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5344989</comments>
            <pubDate>Mon, 24 Oct 2011 23:41:06 +0100</pubDate>
            <guid isPermaLink="false">5344989</guid>        </item>
        <item>
            <title>The connexin mimetic peptide Gap27 increases human dermal fibroblast migration in hyperglycemic and hyperinsulinemic conditions in vitro</title>
            <link>http://www.medworm.com/index.php?rid=5344988&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22705</link>
            <description>AbstractSignificant increases in skin wound healing rates occur by reducing connexin‐mediated communication (CMC). Gap27, a connexin (Cx) mimetic peptide targeted to the second extracellular loop of Cx43, which inhibits CMC, increases migration of human keratinocytes and dermal fibroblasts. To examine the efficacy of Gap27 in a hyperglycemic and hyperinsulinemic in vitro environment, cell migration, gap junction, and Cx hemichannel functionality and cell–substrate adhesion assays were performed on human dermal fibroblasts and diabetic fibroblast and keratinocytes. To investigate fibroblast genes involved in these processes, extra‐cellular matrix (ECM) and adhesion gene expression was determined with a PCR array. Gap27 increased fibroblast migration in both euglycemia/euinsulinemia an...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5344988</comments>
            <pubDate>Mon, 24 Oct 2011 23:40:54 +0100</pubDate>
            <guid isPermaLink="false">5344988</guid>        </item>
        <item>
            <title>Malignant mesothelioma: Facts, Myths, and Hypotheses</title>
            <link>http://www.medworm.com/index.php?rid=5344987&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22724</link>
            <description>AbstractMalignant mesothelioma (MM) is a neoplasm arising from mesothelial cells lining the pleural, peritoneal, and pericardial cavities. Over 20 million people in the US are at risk of developing MM due to asbestos exposure. MM mortality rates are estimated to increase by 5–10% per year in most industrialized countries until about 2020. The incidence of MM in men has continued to rise during the past 50 years, while the incidence in women appears largely unchanged. It is estimated that about 50–80% of pleural MM in men and 20–30% in women developed in individuals whose history indicates asbestos exposure(s) above that expected from most background settings. While rare for women, about 30% of peritoneal mesothelioma in men has been associated with exposure to asbestos. Erionite is a...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5344987</comments>
            <pubDate>Mon, 24 Oct 2011 23:40:50 +0100</pubDate>
            <guid isPermaLink="false">5344987</guid>        </item>
        <item>
            <title>Potential mechanism of interleukin‐8 production from lung cancer cells: An involvement of EGF–EGFR–PI3K–Akt–Erk pathway</title>
            <link>http://www.medworm.com/index.php?rid=5344986&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.22722</link>
            <description>AbstractTumor inflammatory microenvironment is considered to play the role in the sensitivity of tumor cells to therapies and prognosis of lung cancer patients. Interleukin‐8 (IL‐8) is one of critical chemo‐attractants responsible for leukocyte recruitment, cancer proliferation, and angiogenesis. The present study aimed at investigating potential mechanism of IL‐8 production from human non‐small cell lung cancer (NSCLC) SPC‐A1 cells. We initially found that EGF could directly stimulate IL‐8 production, proliferation, and bio‐behaviors of lung cancer cells through the activation of EGFR, PI3K, Akt, and Erk signal pathway. EGF‐stimulated IL‐8 production, phosphorylation of Akt and Erk, and cell proliferation and movement could be inhibited by EGFR inhibitor (Erlotinib), P...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5344986</comments>
            <pubDate>Mon, 24 Oct 2011 23:40:49 +0100</pubDate>
            <guid isPermaLink="false">5344986</guid>        </item>
        <item>
            <title>CASK interacts with PMCA4b and JAM‐A on the mouse sperm flagellum to regulate Ca2+ homeostasis and motility</title>
            <link>http://www.medworm.com/index.php?rid=5344978&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.24000</link>
            <description>AbstractDeletion of the highly conserved gene for the major Ca2+ efflux pump, Plasma membrane calcium/calmodulin‐dependent ATPase 4b (Pmca4b), in the mouse leads to loss of progressive and hyperactivated sperm motility and infertility. Here we first demonstrate that compared to wild‐type (WT), Junctional adhesion molecule‐A (Jam‐A) null sperm, previously shown to have motility defects and an abnormal mitochondrial phenotype reminiscent of that seen in Pmca4b nulls, exhibit reduced (P &amp;lt; 0.001) ATP levels, significantly (P &amp;lt; 0.001) greater cytosolic Ca2+ concentration ([Ca2+]c) and ∼10‐fold higher mitochondrial sequestration, indicating Ca2+ overload. Investigating the mechanism involved, we used co‐immunoprecipitation studies to show that CASK (Ca2+/calmodulin‐...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5344978</comments>
            <pubDate>Mon, 24 Oct 2011 23:34:53 +0100</pubDate>
            <guid isPermaLink="false">5344978</guid>        </item>
        <item>
            <title>Highlights: Volume 226, Number 12</title>
            <link>http://www.medworm.com/index.php?rid=5332899&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23057</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332899</comments>
            <pubDate>Fri, 21 Oct 2011 04:40:13 +0100</pubDate>
            <guid isPermaLink="false">5332899</guid>        </item>
        <item>
            <title>Table of Contents: Volume 226, Number 12</title>
            <link>http://www.medworm.com/index.php?rid=5332898&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23056</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332898</comments>
            <pubDate>Fri, 21 Oct 2011 04:40:11 +0100</pubDate>
            <guid isPermaLink="false">5332898</guid>        </item>
        <item>
            <title>Journal of Cellular Physiology: Volume 226, Number 12, December 2011</title>
            <link>http://www.medworm.com/index.php?rid=5332897&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23055</link>
            <description>AbstractCover: The cover shows cells treated with collagen and staining with Bmi‐1 (green) and propidium iodide (red). See article in this issue by Suh and Han, pages 3422–3432. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332897</comments>
            <pubDate>Fri, 21 Oct 2011 04:40:10 +0100</pubDate>
            <guid isPermaLink="false">5332897</guid>        </item>
        <item>
            <title>Angiopoietin‐1 but not angiopoietin‐2 induces IL‐8 synthesis and release by human neutrophils</title>
            <link>http://www.medworm.com/index.php?rid=5332885&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23061</link>
            <description>AbstractWe previously reported Tie2 receptor expression on human neutrophils, which promotes chemotactic activities upon activation by both angiopoietins (Ang1 and Ang2). Moreover, we observed that neutrophil pretreatment with Ang1 or Ang2 enhances IL‐8 chemotactic effect. Therefore, we assessed the capacity of Ang1 and/or Ang2 to modulate neutrophil IL‐8 synthesis and release. Neutrophils isolated from healthy donors were stimulated in a time‐ (1‐6 hours) and concentration‐ (10−10‐10−8 M) dependent manner with both angiopoietins. IL‐8 mRNA production was measured by RT‐qPCR, whereas its protein synthesis and release from neutrophils was assessed by ELISA. Ang1 (10−8 M) induced a significant and maximal increase of IL‐8 mRNA (4.7‐fold) within 1 hour, and pro...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332885</comments>
            <pubDate>Fri, 21 Oct 2011 04:33:51 +0100</pubDate>
            <guid isPermaLink="false">5332885</guid>        </item>
        <item>
            <title>Endoplasmic reticulum‐specific BH3‐only protein BNIP1 induces mitochondrial fragmentation in a Bcl‐2‐ and Drp1‐dependent manner</title>
            <link>http://www.medworm.com/index.php?rid=5332896&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23044</link>
            <description>AbstractBcl‐2/adenovirus E1B 19‐kDa interacting protein 1 (BNIP1), which is predominantly localized to the endoplasmic reticulum (ER), is a pro‐apoptotic Bcl‐2 homology domain 3 (BH3)‐only protein. Here, we show that the expression of BNIP1 induced not only a highly interconnected ER network but also mitochondrial fragmentation in a BH3 domain‐dependent manner. Functional analysis demonstrated that BNIP1 expression increased dynamin‐related protein 1 (Drp1) expression followed by the mitochondrial translocation of Drp1 and subsequent mitochondrial fission. Both BNIP1‐induced mitochondrial fission and the translocation of Drp1 were abrogated by Bcl‐2 overexpression. These results collectively indicate that ER‐specific BNIP1 plays an important role in mitochondrial dynami...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332896</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5332896</guid>        </item>
        <item>
            <title>Branch chain amino acid, insulin and hepatic tumor cell proliferation</title>
            <link>http://www.medworm.com/index.php?rid=5332895&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23047</link>
            <description>(Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332895</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5332895</guid>        </item>
        <item>
            <title>The phosphoinositide 3'‐kinase p110δ modulates contractile protein production and IL‐6 release in human airway smooth muscle</title>
            <link>http://www.medworm.com/index.php?rid=5332894&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23046</link>
            <description>Conclusion: PI3K p110δ is important for TGFβ1 induced production of the contractile proteins calponin and α‐SMA and the proinflammatory cytokine IL‐6 in ASM cells, and may therefore be relevant as a potential therapeutic target to treat both inflammation and airway remodeling. J. Cell. Physiol. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332894</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5332894</guid>        </item>
        <item>
            <title>Regulation of asthmatic airway relaxation by estrogen and heat shock protein 90</title>
            <link>http://www.medworm.com/index.php?rid=5332893&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23045</link>
            <description>AbstractWe tested the hypothesis that asthmatic mouse airways exhibit impaired relaxation to NO donors. Mouse tracheal rings were incubated overnight in serum from asthmatic human subjects or from non‐asthmatic controls. The next day, cumulative concentration‐response curves (CCRC) to sodium nitroprusside (SNP) and nitroglycerine (NTG) were obtained. Both SNP and NTG relaxed the pre‐constricted normal tracheal rings. Tracheal rings exposed to serum from asthmatic patients exhibited a more than a 3‐fold increase in the EC50 of SNP and NTG. Pre‐incubation of tracheal rings with heat shock protein 90 inhibitors decreased the relaxation of both normal and asthmatic tracheal rings to SNP and NTG. Pre‐incubation with estradiol did not affect normal tracheal ring relaxation but exhibi...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332893</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5332893</guid>        </item>
        <item>
            <title>Emerging role of angiogenin in stress response and cell survival under adverse conditions</title>
            <link>http://www.medworm.com/index.php?rid=5332892&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23051</link>
            <description>AbstractAngiogenin (ANG), also known as ribonuclease (RNASE) 5, is a member of the vertebrate‐specific, secreted RNASE superfamily. ANG was originally identified as a tumor angiogenic factor, but its biological activity has been extended from inducing angiogenesis to stimulating cell proliferation and more recently, to promoting cell survival. Under growth conditions, ANG is translocated to nucleus where it accumulates in nucleolus and stimulates ribosomal RNA (rRNA) transcription, thus facilitating cell growth and proliferation. Under stress conditions, ANG is accumulated in cytoplasmic compartments and modulates the production of tiRNA, a novel class of small RNA that is derived from tRNA and is induced by stress. tiRNA suppress global protein translation by inhibiting both cap‐depen...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332892</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5332892</guid>        </item>
        <item>
            <title>Ganoderma lucidum polysaccharides prevent platelet‐derived growth factor‐stimulated smooth muscle cell proliferation in vitro and neointimal hyperplasia in the endothelial‐denuded artery in vivo</title>
            <link>http://www.medworm.com/index.php?rid=5332891&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23053</link>
            <description>AbstractGanoderma lucidum is used in traditional Chinese medicine to prevent or treat a variety of diseases, including cardiovascular disorders. We previously demonstrated that a glucan‐containing extract of Reishi polysaccharides (EORP) has the potent anti‐inflammatory action of reducing ICAM‐1 expression in lipopolysaccharide (LPS)‐treated human aortic endothelial cells (HASMCs) and LPS‐treated mice. In the present study, we examined whether EORP inhibited platelet‐derived growth factor‐BB (PDGF)‐stimulated HASMC proliferation and the mechanism involved. EORP dose‐dependently reduced cell numbers and DNA synthesis of PDGF‐treated HASMCs in vitro. EORP also arrested cell cycle progression in the G0/G1 phase, and this was associated with decreased expression of cyclin D...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332891</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5332891</guid>        </item>
        <item>
            <title>AMP‐activated protein kinase mediates erythropoietin‐induced activation of endothelial nitric oxide synthase</title>
            <link>http://www.medworm.com/index.php?rid=5332890&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23052</link>
            <description>AbstractWe investigated whether AMP‐activated protein kinase (AMPK), a multi‐functional regulator of energy homeostasis, participates in the regulation of erythropoietin (EPO)‐mediated activation of endothelial nitric oxide synthase (eNOS) in endothelial cells (ECs) and mice. In ECs, treatment with EPO increased the phosphorylation of AMPK, acetyl‐CoA carboxylase (ACC) and eNOS, as revealed by western blot analysis. Inhibition of AMPK activation by compound C or dominant‐negative AMPK mutant abrogated the EPO‐induced increase in the phosphorylation of AMPK, ACC and eNOS, as well as nitric oxide (NO) production. Additionally, suppression of AMPK activation abolished EPO‐induced EC proliferation, migration and tube formation. Immunoprecipitation analysis demonstrated that AMPK ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332890</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5332890</guid>        </item>
        <item>
            <title>Monocytes differentiation upon treatment with a peptide corresponding to the C‐terminus of activated T cell‐expressed Tirc7 protein</title>
            <link>http://www.medworm.com/index.php?rid=5332889&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23059</link>
            <description>In conclusion, we report for the first time on biological effects mediated by a peptide corresponding to the C‐terminus of Tirc7 protein, which interfere with monocytic differentiation pathways. J. Cell. Physiol. © 2011 Wiley Periodicals, Inc. (Source: Journal of Cellular Physiology)</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332889</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5332889</guid>        </item>
        <item>
            <title>Gender related alterations of β‐adrenoceptor mechanisms in heart failure due to arteriovenous fistula</title>
            <link>http://www.medworm.com/index.php?rid=5332888&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23058</link>
            <description>This study was undertaken to determine gender related changes in different components of β‐adrenoceptor (β‐AR) system in response to arteriovenous fistula (AV‐shunt), which is known to produce heart failure due to volume overload. AV‐shunt was induced in male and female rats for 16 wks by the needle technique; ovariectomized (OVX) rats treated with or without estrogen were also used. Although AV‐shunt for 16 wks produced cardiac hypertrophy in both sexes, male animals showed cardiac dysfunction whereas cardiac performance was maintained in females. Both β1‐AR and β2‐AR protein content and mRNA levels were decreased in male and increased in female hearts post‐AV‐shunt. The basal adenylyl cyclase (AC) activity was lower in the female heart; however, AC protein content a...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332888</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5332888</guid>        </item>
        <item>
            <title>Proteasome modulator 9 is linked to microvascular pathology of T2D</title>
            <link>http://www.medworm.com/index.php?rid=5332887&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23063</link>
            <description>AbstractThe locus 12q24 is linked to type 2 diabetes (T2D) and to changes in retinal vascular caliber in Caucasians. Proteasome Modulator 9 gene (PSMD9) lies in the 12q24 locus and is implicated diabetes onset and in degradation of intracellular proteins in antigenic peptides in the immune response to antigen presentation by MHC class I cells. Within PSMD9, we reported a linkage to T2D and to MODY3 in Italian families. We recently demonstrated a linkage of the PSMD9 T2D risk SNPs with T2D‐nephropathy, T2D‐neuropathy, retinopathy, hypercholesterolemia, and macrovascular pathology.We aimed at studying the presence of the linkage signal of the PSMD9 T2D risk SNPs IVS3 + nt460, IVS3 + nt437, E197G to microvascular pathology associated to T2D Italian siblings/families.We screened 20...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332887</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5332887</guid>        </item>
        <item>
            <title>Inhibition of long term potention by CuZn superoxide dismutase injection in rat dentate gyrus : Involvement of muscarinic M1 receptor</title>
            <link>http://www.medworm.com/index.php?rid=5332886&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23062</link>
            <description>AbstractLong term potentiation and long term depression represent important processes that modulate synaptic transmission that carries out a key role in neural mechanisms of memory.Many studies give strong evidences on a role of the reactive oxygen species in the induction of LTP in CA1 region of hippocampal slices that was inhibited by adding the scavenger enzyme superoxide dismutase (SOD1).Previous data showed that SOD1 is secreted by many cellular lines, including neuroblastoma SK‐N‐BE cells through microvesicles by an ATP dependent mechanism; moreover, it has been shown that SOD1 interacts with human neuroblastoma cell membranes increasing intracellular calcium levels via a phospholipase C‐protein kinase C pathway activation.The aim of this study was to investigate the effect of ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5332886</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5332886</guid>        </item>
        <item>
            <title>Identification of proteins that associate with integrin α2 by proteomic analysis in human fibrosarcoma HT‐1080 cells</title>
            <link>http://www.medworm.com/index.php?rid=5312305&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23054</link>
            <description>In this study, we expressed integrin α2 fused at the C terminus to a FLAG peptide in HT1080 cells. Cells stably expressing the chimeric protein were lysed with 1% Brij‐98 and affinity purified using anti‐FLAG antibody. Integrin β1 co‐purified with integrin α2 confirming the specificity of the purification procedure. Analysis of the purified mixture by nano‐LC/MS/MS identified 70 proteins. Nineteen of these were membrane proteins, including adhesion proteins, receptors, transporters, proteinases, and ion channel receptors, and the balance were cytoplasmic. Interestingly, eight of the proteins had previously been shown to associate with MT1‐MMP. We believe the present study provides a platform to facilitate the study of the mechanisms of cell adhesion, migration and invasion. ...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5312305</comments>
            <pubDate>Fri, 14 Oct 2011 03:10:45 +0100</pubDate>
            <guid isPermaLink="false">5312305</guid>        </item>
        <item>
            <title>Pathophysiology of stroke and stroke induced retinal ischemia: Emerging role of stem cells</title>
            <link>http://www.medworm.com/index.php?rid=5312306&amp;cid=s_33777_171_f&amp;fid=33777&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fjcp.23048</link>
            <description>AbstractThe current review focuses on pathophysiology, animal models and molecular analysis of stroke and retinal ischemia, and the role of stem cells in recovery of these disease conditions. Research findings associated with ischemic stroke and retinal ischemia have been discussed, and efforts towards prevention and limiting the recurrence of ischemic diseases, as well as emerging treatment possibilities with endothelial progenitor cells in ischemic diseases, are presented. Although most neurological diseases are still not completely understood and reliable treatment is lacking, animal models provide a major step in validating novel therapies. Stem cell approaches constitute an emerging form of cell‐based therapy to treat ischemic diseases since it is an attractive source for regenerati...</description>
            <author>Journal of Cellular Physiology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5312306</comments>
            <pubDate>Tue, 11 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5312306</guid>        </item>
    </channel>
</rss>

