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10.1038/s41598-017-05624-2 http://scihub22266oqcxt.onion/10.1038/s41598-017-05624-2 C5511333!5511333 !28710437     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28710437 &cmd=llinks): Failed to open stream: HTTP request failed! 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Inhibition of CTGF ameliorates peritoneal fibrosis through suppression of fibroblast and myofibroblast accumulation and angiogenesis |pdf=|usr=}}{{28710437 }} gab.com Text Inhibition of CTGF ameliorates peritoneal fibrosis through suppression of fibroblast and myofibroblast accumulation and angiogenesis JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28710437 #FOAvip Peritoneal fibrosis (PF) is a serious complication in various clinical settings, but the mechanisms driving it remain to be fully determined. Connective tissue growth factor (CTGF) is known to regulate fibroblast activities. We therefore examined if CTGF inhibition has anti-fibrotic effects in PF. PF was induced by repetitive intraperitoneal injections of chlorhexidine gluconate (CG) in mice with type I pro-collagen promoter-driven green fluorescent protein (GFP) expression to identify fibroblasts. FG-3019, an anti-CTGF monoclonal antibody, was used to inhibit CTGF. CG-induced PF was significantly attenuated in FG-3019-treated mice. CG challenges induced marked accumulations of proliferating fibroblasts and of myofibroblasts, which were both reduced by FG-3019. Levels of peritoneal CTGF expression were increased by CG challenges, and suppressed in FG-3019-treated mice. FG-3019 treatment also reduced the number of CD31(+) vessels and VEGF-A-positive cells in fibrotic peritoneum. In vitro studies using NIH 3T3 fibroblasts and peritoneal mesothelial cells (PMCs) showed that CTGF blockade suppressed TGF-?(1)-induced fibroblast proliferation and myofibroblast differentiation, PMC mesothelial-to-mesenchymal transition, and VEGF-A production. These findings suggest that the inhibition of CTGF by FG-3019 might be a novel treatment for PF through the regulation of fibroblast and myofibroblast accumulation and angiogenesis. Twit Text FOAVip Inhibition of CTGF ameliorates peritoneal fibrosis through suppression of fibroblast and myofibroblast accumulation and angiogenesis ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28710437 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28710437 #FOAvip English Wikipedia <ref>{{Cite pmid|28710437 }}</ref> Inhibition of CTGF ameliorates peritoneal fibrosis through suppression of fibroblast and myofibroblast accumulation and angiogenesis #MMPMID28710437 Sakai N ; Nakamura M ; Lipson KE ; Miyake T ; Kamikawa Y ; Sagara A ; Shinozaki Y ; Kitajima S ; Toyama T ; Hara A ; Iwata Y ; Shimizu M ; Furuichi K ; Kaneko S ; Tager AM ; Wada T Sci Rep 2017[Jul]; 7 (1 ): 5392 PMID28710437 show ga Peritoneal fibrosis (PF) is a serious complication in various clinical settings, but the mechanisms driving it remain to be fully determined. Connective tissue growth factor (CTGF) is known to regulate fibroblast activities. We therefore examined if CTGF inhibition has anti-fibrotic effects in PF. PF was induced by repetitive intraperitoneal injections of chlorhexidine gluconate (CG) in mice with type I pro-collagen promoter-driven green fluorescent protein (GFP) expression to identify fibroblasts. FG-3019, an anti-CTGF monoclonal antibody, was used to inhibit CTGF. CG-induced PF was significantly attenuated in FG-3019-treated mice. CG challenges induced marked accumulations of proliferating fibroblasts and of myofibroblasts, which were both reduced by FG-3019. Levels of peritoneal CTGF expression were increased by CG challenges, and suppressed in FG-3019-treated mice. FG-3019 treatment also reduced the number of CD31(+) vessels and VEGF-A-positive cells in fibrotic peritoneum. In vitro studies using NIH 3T3 fibroblasts and peritoneal mesothelial cells (PMCs) showed that CTGF blockade suppressed TGF-?(1)-induced fibroblast proliferation and myofibroblast differentiation, PMC mesothelial-to-mesenchymal transition, and VEGF-A production. These findings suggest that the inhibition of CTGF by FG-3019 might be a novel treatment for PF through the regulation of fibroblast and myofibroblast accumulation and angiogenesis. |Angiogenesis Inhibitors/*pharmacology [MESH] |Animals [MESH] |Antibodies, Monoclonal, Humanized [MESH] |Antibodies, Monoclonal/*pharmacology [MESH] |Cell Differentiation/drug effects [MESH] |Chlorhexidine/analogs & derivatives [MESH] |Collagen Type I/genetics/metabolism [MESH] |Connective Tissue Growth Factor/antagonists & inhibitors/*genetics/metabolism [MESH] |Disease Models, Animal [MESH] |Fibroblasts/drug effects/metabolism/pathology [MESH] |Gene Expression Regulation [MESH] |Genes, Reporter [MESH] |Green Fluorescent Proteins/genetics/metabolism [MESH] |Humans [MESH] |Mice [MESH] |Mice, Transgenic [MESH] |Myofibroblasts/drug effects/metabolism/pathology [MESH] |NIH 3T3 Cells [MESH] |Neovascularization, Pathologic/chemically induced/genetics/pathology/*prevention & control [MESH] |Peritoneal Fibrosis/chemically induced/*drug therapy/genetics/pathology [MESH] |Signal Transduction [MESH] |Transforming Growth Factor beta1/genetics/metabolism [MESH]Inhibition of CTGF ameliorates peritoneal fibrosis through suppression(epmc).pdf DeepDyve Pubget Overpricing