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10.1172/jci.insight.85717 http://scihub22266oqcxt.onion/10.1172/jci.insight.85717 C4922427!4922427 !27358914     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27358914 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       JCI+Insight 2016 ; 1 (8 ): ä Nephropedia Template TP {{tp|p=27358914 |t=2016. Attenuation of lung fibrosis in mice with a clinically relevant inhibitor of glutathione-S-transferase ? |pdf=|usr=}}{{27358914 }} gab.com Text Attenuation of lung fibrosis in mice with a clinically relevant inhibitor of glutathione-S-transferase JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=27358914 #FOAvip Idiopathic pulmonary fibrosis (IPF) is a debilitating lung disease characterized by excessive collagen production and fibrogenesis. Apoptosis in lung epithelial cells is critical in IPF pathogenesis, as heightened loss of these cells promotes fibroblast activation and remodeling. Changes in glutathione redox status have been reported in IPF patients. S-glutathionylation, the conjugation of glutathione to reactive cysteines, is catalyzed in part by glutathione-S-transferase ? (GSTP). To date, no published information exists linking GSTP and IPF to our knowledge. We hypothesized that GSTP mediates lung fibrogenesis in part through FAS S-glutathionylation, a critical event in epithelial cell apoptosis. Our results demonstrate that GSTP immunoreactivity is increased in the lungs of IPF patients, notably within type II epithelial cells. The FAS-GSTP interaction was also increased in IPF lungs. Bleomycin- and AdTGF?-induced increases in collagen content, ?-SMA, FAS S-glutathionylation, and total protein S-glutathionylation were strongly attenuated in Gstp(-/-) mice. Oropharyngeal administration of the GSTP inhibitor, TLK117, at a time when fibrosis was already apparent, attenuated bleomycin- and AdTGF?-induced remodeling, ?-SMA, caspase activation, FAS S-glutathionylation, and total protein S-glutathionylation. GSTP is an important driver of protein S-glutathionylation and lung fibrosis, and GSTP inhibition via the airways may be a novel therapeutic strategy for the treatment of IPF. Twit Text FOAVip Attenuation of lung fibrosis in mice with a clinically relevant inhibitor of glutathione-S-transferase ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=27358914 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27358914 #FOAvip English Wikipedia <ref>{{Cite pmid|27358914 }}</ref> Attenuation of lung fibrosis in mice with a clinically relevant inhibitor of glutathione-S-transferase ? #MMPMID27358914 McMillan DH ; van der Velden JL ; Lahue KG ; Qian X ; Schneider RW ; Iberg MS ; Nolin JD ; Abdalla S ; Casey DT ; Tew KD ; Townsend DM ; Henderson CJ ; Wolf CR ; Butnor KJ ; Taatjes DJ ; Budd RC ; Irvin CG ; van der Vliet A ; Flemer S ; Anathy V ; Janssen-Heininger YM JCI Insight 2016[Jun]; 1 (8 ): ä PMID27358914 show ga Idiopathic pulmonary fibrosis (IPF) is a debilitating lung disease characterized by excessive collagen production and fibrogenesis. Apoptosis in lung epithelial cells is critical in IPF pathogenesis, as heightened loss of these cells promotes fibroblast activation and remodeling. Changes in glutathione redox status have been reported in IPF patients. S-glutathionylation, the conjugation of glutathione to reactive cysteines, is catalyzed in part by glutathione-S-transferase ? (GSTP). To date, no published information exists linking GSTP and IPF to our knowledge. We hypothesized that GSTP mediates lung fibrogenesis in part through FAS S-glutathionylation, a critical event in epithelial cell apoptosis. Our results demonstrate that GSTP immunoreactivity is increased in the lungs of IPF patients, notably within type II epithelial cells. The FAS-GSTP interaction was also increased in IPF lungs. Bleomycin- and AdTGF?-induced increases in collagen content, ?-SMA, FAS S-glutathionylation, and total protein S-glutathionylation were strongly attenuated in Gstp(-/-) mice. Oropharyngeal administration of the GSTP inhibitor, TLK117, at a time when fibrosis was already apparent, attenuated bleomycin- and AdTGF?-induced remodeling, ?-SMA, caspase activation, FAS S-glutathionylation, and total protein S-glutathionylation. GSTP is an important driver of protein S-glutathionylation and lung fibrosis, and GSTP inhibition via the airways may be a novel therapeutic strategy for the treatment of IPF. äAttenuation of lung fibrosis in mice with a clinically relevant inhibi(epmc).pdf DeepDyve Pubget Overpricing