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10.1016/j.jaut.2015.07.010 http://scihub22266oqcxt.onion/10.1016/j.jaut.2015.07.010 C4644665!4644665 !26238209     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26238209 &cmd=llinks): Failed to open stream: HTTP request failed! 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Treatment of cholestatic fibrosis by altering gene expression of Cthrc1: Implications for autoimmune and non-autoimmune liver disease |pdf=|usr=}}{{26238209 }} gab.com Text Treatment of cholestatic fibrosis by altering gene expression of Cthrc1: Implications for autoimmune and non-autoimmune liver disease JO: J Autoimmun http://www.kidney.de/pget.php?&tw=1&pmid=26238209 #FOAvip Collagen triple helix repeat containing-1 (Cthrc1) is a documented specific inhibitor of TGF-? signaling. Based on this observation, we developed the hypothesis that knocking in/knocking out the Cthrc1 gene in murine models of cholestasis would alter the natural history of cholestatic fibrosis. To study this thesis, we studied two murine models of fibrosis, first, common bile duct ligation (CBDL) and second, feeding of 3, 5-diethoxy-carbonyl-1, 4-dihydrocollidine (DDC). In both models, we administered well-defined adenoviral vectors that expressed either Cthrc1 or, alternatively, a short hairpin RNA (shRNA)-targeting Cthrc1 either before or after establishment of fibrosis. Importantly, when Cthrc1 gene expression was enhanced, we noted a significant improvement of hepatic fibrosis, both microscopically and by analysis of fibrotic gene expression. In contrast, when Cthrc1 gene expression was deleted, there was a significant exacerbation of fibrosis. To identify the mechanism of action of these significant effects produced by knocking in/knocking out Cthrc gene expression, we thence studied the interaction of Cthrc1 gene expression using hepatic stellate cells (HSCs) and human LX-2 cells. Importantly, we demonstrate that Cthrc1 is induced by TGF-?1 via phospho-Smad3 binding to the promoter with subsequent transcription activation. In addition, we demonstrate that Cthrc1 inhibits TGF-? signaling by accelerating degradation of phospho-Smad3 through a proteosomal pathway. Importantly, the anti-fibrotic effects can be recapitulated with a truncated fragment of Cthrc1. In conclusion, our findings uncover a critical negative feedback regulatory loop in which TGF-?1 induces Cthrc1, which can attenuate fibrosis by accelerating degradation of phospho-Smad3. Twit Text FOAVip Treatment of cholestatic fibrosis by altering gene expression of Cthrc1: Implications for autoimmune and non-autoimmune liver disease ????J Autoimmun http://www.kidney.de/pget.php?&tw=1&pmid=26238209 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26238209 #FOAvip English Wikipedia <ref>{{Cite pmid|26238209 }}</ref> Treatment of cholestatic fibrosis by altering gene expression of Cthrc1: Implications for autoimmune and non-autoimmune liver disease #MMPMID26238209 Bian Z ; Miao Q ; Zhong W ; Zhang H ; Wang Q ; Peng Y ; Chen X ; Guo C ; Shen L ; Yang F ; Xu J ; Qiu D ; Fang J ; Friedman S ; Tang R ; Gershwin ME ; Ma X J Autoimmun 2015[Sep]; 63 (ä): 76-87 PMID26238209 show ga Collagen triple helix repeat containing-1 (Cthrc1) is a documented specific inhibitor of TGF-? signaling. Based on this observation, we developed the hypothesis that knocking in/knocking out the Cthrc1 gene in murine models of cholestasis would alter the natural history of cholestatic fibrosis. To study this thesis, we studied two murine models of fibrosis, first, common bile duct ligation (CBDL) and second, feeding of 3, 5-diethoxy-carbonyl-1, 4-dihydrocollidine (DDC). In both models, we administered well-defined adenoviral vectors that expressed either Cthrc1 or, alternatively, a short hairpin RNA (shRNA)-targeting Cthrc1 either before or after establishment of fibrosis. Importantly, when Cthrc1 gene expression was enhanced, we noted a significant improvement of hepatic fibrosis, both microscopically and by analysis of fibrotic gene expression. In contrast, when Cthrc1 gene expression was deleted, there was a significant exacerbation of fibrosis. To identify the mechanism of action of these significant effects produced by knocking in/knocking out Cthrc gene expression, we thence studied the interaction of Cthrc1 gene expression using hepatic stellate cells (HSCs) and human LX-2 cells. Importantly, we demonstrate that Cthrc1 is induced by TGF-?1 via phospho-Smad3 binding to the promoter with subsequent transcription activation. In addition, we demonstrate that Cthrc1 inhibits TGF-? signaling by accelerating degradation of phospho-Smad3 through a proteosomal pathway. Importantly, the anti-fibrotic effects can be recapitulated with a truncated fragment of Cthrc1. In conclusion, our findings uncover a critical negative feedback regulatory loop in which TGF-?1 induces Cthrc1, which can attenuate fibrosis by accelerating degradation of phospho-Smad3. |*Gene Expression Regulation [MESH] |Animals [MESH] |Autoimmune Diseases/genetics/therapy [MESH] |Cell Line [MESH] |Cholestasis, Intrahepatic/genetics/*therapy [MESH] |Extracellular Matrix Proteins/*genetics/metabolism [MESH] |Genetic Therapy [MESH] |Hepatic Stellate Cells/immunology/*metabolism [MESH] |Humans [MESH] |Liver Cirrhosis/genetics/therapy [MESH] |Liver Diseases [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Pyridines [MESH] |Smad3 Protein/*metabolism [MESH]Treatment of cholestatic fibrosis by altering gene expression of Cthrc(epmc).pdf DeepDyve Pubget Overpricing