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10.1371/journal.pone.0186740 http://scihub22266oqcxt.onion/10.1371/journal.pone.0186740 C5648211!5648211 !29049376     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29049376 &cmd=llinks): Failed to open stream: HTTP request failed! 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Antioxidants and NOX1/NOX4 inhibition blocks TGF?1-induced CCN2 and ?-SMA expression in dermal and gingival fibroblasts |pdf=|usr=}}{{29049376 }} gab.com Text Antioxidants and NOX1/NOX4 inhibition blocks TGF 1-induced CCN2 and -SMA expression in dermal and gingival fibroblasts JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29049376 #FOAvip TGFbeta induces fibrogenic responses in fibroblasts. Reactive oxygen species (ROS)/nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) may contribute to fibrogenic responses. Here, we examine if the antioxidant N-acetylcysteine (NAC), the NOX inhibitor diphenyleneiodonium (DPI) and the selective NOX1/NOX4 inhibitor GKT-137831 impairs the ability of TGFbeta to induce profibrotic gene expression in human gingival (HGF) and dermal (HDF) fibroblasts. We also assess if GKT-137831 can block the persistent fibrotic phenotype of lesional scleroderma (SSc) fibroblasts. We use real-time polymerase chain reaction and Western blot analysis to evaluate whether NAC and DPI impair the ability of TGFbeta1 to induce expression of fibrogenic genes in fibroblasts. The effects of GKT-137831 on TGFbeta-induced protein expression and the persistent fibrotic phenotype of lesional scleroderma (SSc) fibroblasts were tested using Western blot and collagen gel contraction analyses. In HDF and HGF, TGFbeta1 induces CCN2, CCN1, endothelin-1 and alpha-smooth muscle actin (SMA) in a fashion sensitive to NAC. Induction of COL1A1 mRNA was unaffected. Similar results were seen with DPI. NAC and DPI impaired the ability of TGFbeta1 to induce protein expression of CCN2 and alpha-SMA in HDF and HGF. GKT-137831 impaired TGFbeta-induced CCN2 and alpha-SMA protein expression in HGF and HDF. In lesional SSc dermal fibroblasts, GKT-137831 reduced alpha-SMA and CCN2 protein overexpression and collagen gel contraction. These results are consistent with the hypothesis that antioxidants or NOX1/4 inhibition may be useful in blocking profibrotic effects of TGFbeta on dermal and gingival fibroblasts and warrant consideration for further development as potential antifibrotic agents. Twit Text FOAVip Antioxidants and NOX1/NOX4 inhibition blocks TGF 1-induced CCN2 and -SMA expression in dermal and gingival fibroblasts ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29049376 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29049376 #FOAvip English Wikipedia <ref>{{Cite pmid|29049376 }}</ref> Antioxidants and NOX1/NOX4 inhibition blocks TGF?1-induced CCN2 and ?-SMA expression in dermal and gingival fibroblasts #MMPMID29049376 Murphy-Marshman H ; Quensel K ; Shi-Wen X ; Barnfield R ; Kelly J ; Peidl A ; Stratton RJ ; Leask A PLoS One 2017[]; 12 (10 ): e0186740 PMID29049376 show ga TGFbeta induces fibrogenic responses in fibroblasts. Reactive oxygen species (ROS)/nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) may contribute to fibrogenic responses. Here, we examine if the antioxidant N-acetylcysteine (NAC), the NOX inhibitor diphenyleneiodonium (DPI) and the selective NOX1/NOX4 inhibitor GKT-137831 impairs the ability of TGFbeta to induce profibrotic gene expression in human gingival (HGF) and dermal (HDF) fibroblasts. We also assess if GKT-137831 can block the persistent fibrotic phenotype of lesional scleroderma (SSc) fibroblasts. We use real-time polymerase chain reaction and Western blot analysis to evaluate whether NAC and DPI impair the ability of TGFbeta1 to induce expression of fibrogenic genes in fibroblasts. The effects of GKT-137831 on TGFbeta-induced protein expression and the persistent fibrotic phenotype of lesional scleroderma (SSc) fibroblasts were tested using Western blot and collagen gel contraction analyses. In HDF and HGF, TGFbeta1 induces CCN2, CCN1, endothelin-1 and alpha-smooth muscle actin (SMA) in a fashion sensitive to NAC. Induction of COL1A1 mRNA was unaffected. Similar results were seen with DPI. NAC and DPI impaired the ability of TGFbeta1 to induce protein expression of CCN2 and alpha-SMA in HDF and HGF. GKT-137831 impaired TGFbeta-induced CCN2 and alpha-SMA protein expression in HGF and HDF. In lesional SSc dermal fibroblasts, GKT-137831 reduced alpha-SMA and CCN2 protein overexpression and collagen gel contraction. These results are consistent with the hypothesis that antioxidants or NOX1/4 inhibition may be useful in blocking profibrotic effects of TGFbeta on dermal and gingival fibroblasts and warrant consideration for further development as potential antifibrotic agents. |Actins/*metabolism [MESH] |Antioxidants/*pharmacology [MESH] |Cells, Cultured [MESH] |Connective Tissue Growth Factor/*metabolism [MESH] |Fibroblasts/metabolism [MESH] |Gingiva/cytology/*metabolism [MESH] |Humans [MESH] |NADPH Oxidase 1/*antagonists & inhibitors [MESH] |NADPH Oxidase 4/*antagonists & inhibitors [MESH] |Skin/cytology/*metabolism [MESH]Antioxidants and NOX1/NOX4 inhibition blocks TGF?1-induced CCN2 and ?-(epmc).pdf DeepDyve Pubget Overpricing