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10.1016/j.exer.2015.06.028 http://scihub22266oqcxt.onion/10.1016/j.exer.2015.06.028 C4553125!4553125!26142957     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26142957&cmd=llinks): Failed to open stream: HTTP request failed! 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Inhibitory effects of PPAR? ligands on TGF-?1-induced CTGF expression in cat corneal fibroblasts |pdf=|usr=}}{{26142957}} gab.com Text Inhibitory effects of PPAR ligands on TGF- 1-induced CTGF expression in cat corneal fibroblasts JO: Exp Eye Res http://www.kidney.de/pget.php?&tw=1&pmid=26142957 #FOAvip Ligands of Peroxisome Proliferator Activated Receptor gamma (PPAR?) possess strong anti-fibrotic properties in the cornea and several other body tissues. In the cornea, we recently showed this class of molecules to prevent stromal myofibroblast differentiation partially by blocking the actions of p38 mitogen-activated protein kinase (MAPK). However, given the important role assigned to connective tissue growth factor (CTGF) in mediating corneal fibrosis, here we asked whether PPAR? ligands also act by affecting transforming growth factor-? (TGF-? 1-induced expression of CTGF in cultured corneal fibroblasts. Corneal keratocytes were isolated from young, adult cats and early passage cells were exposed to TGF-?1 with or without the PPAR? ligands Rosiglitazone, Troglitazone and 15d-PGJ2. Western blots were used to assay levels of CTGF and alpha smooth muscle actin (?SMA), a marker of myofibroblast differentiation. CTGF siRNA demonstrated a critical role for CTGF in TGF-?1-mediated myofibroblast differentiation, while exogenously applied CTGF potentiated the pro-fibrogenic effects of TGF-?1. TGF-?1-mediated increases in CTGF and ?SMA expression were strongly inhibited by all three PPAR? ligands tested, and by a c-jun N-terminal kinase (JNK) inhibitor. However, while extracellular signal-regulated kinase (ERK) 1/2, protein kinase B (AKT) and p38 MAPK inhibitors also blocked TGF-?1-induced ?SMA induction, they did not dampen TGF-?1-induced increases in levels of CTGF. Thus, we conclude that PPAR? ligands block TGF-?-induced increases in CTGF levels in cat corneal fibroblasts. They appear to do this in addition to their anti-fibrotic effect on p38 MAPK, providing a second intracellular pathway by which PPAR? ligands block ?SMA induction. Twit Text FOAVip Inhibitory effects of PPAR ligands on TGF- 1-induced CTGF expression in cat corneal fibroblasts ????Exp Eye Res http://www.kidney.de/pget.php?&tw=1&pmid=26142957 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26142957 #FOAvip English Wikipedia <ref>{{Cite pmid|26142957}}</ref> Inhibitory effects of PPAR? ligands on TGF-?1-induced CTGF expression in cat corneal fibroblasts #MMPMID26142957 Jeon KI; Phipps RP; Sime PJ; Huxlin KR Exp Eye Res 2015[Sep]; 138 (ä): 52-8 PMID26142957show ga Ligands of Peroxisome Proliferator Activated Receptor gamma (PPAR?) possess strong anti-fibrotic properties in the cornea and several other body tissues. In the cornea, we recently showed this class of molecules to prevent stromal myofibroblast differentiation partially by blocking the actions of p38 mitogen-activated protein kinase (MAPK). However, given the important role assigned to connective tissue growth factor (CTGF) in mediating corneal fibrosis, here we asked whether PPAR? ligands also act by affecting transforming growth factor-? (TGF-? 1-induced expression of CTGF in cultured corneal fibroblasts. Corneal keratocytes were isolated from young, adult cats and early passage cells were exposed to TGF-?1 with or without the PPAR? ligands Rosiglitazone, Troglitazone and 15d-PGJ2. Western blots were used to assay levels of CTGF and alpha smooth muscle actin (?SMA), a marker of myofibroblast differentiation. CTGF siRNA demonstrated a critical role for CTGF in TGF-?1-mediated myofibroblast differentiation, while exogenously applied CTGF potentiated the pro-fibrogenic effects of TGF-?1. TGF-?1-mediated increases in CTGF and ?SMA expression were strongly inhibited by all three PPAR? ligands tested, and by a c-jun N-terminal kinase (JNK) inhibitor. However, while extracellular signal-regulated kinase (ERK) 1/2, protein kinase B (AKT) and p38 MAPK inhibitors also blocked TGF-?1-induced ?SMA induction, they did not dampen TGF-?1-induced increases in levels of CTGF. Thus, we conclude that PPAR? ligands block TGF-?-induced increases in CTGF levels in cat corneal fibroblasts. They appear to do this in addition to their anti-fibrotic effect on p38 MAPK, providing a second intracellular pathway by which PPAR? ligands block ?SMA induction. äInhibitory effects of PPAR? ligands on TGF-?1-induced CTGF expression (epmc).pdf DeepDyve Pubget Overpricing