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10.4049/jimmunol.1400861 http://scihub22266oqcxt.onion/10.4049/jimmunol.1400861 C4185218!4185218 !25210118     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25210118 &cmd=llinks): Failed to open stream: HTTP request failed! 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IL-17A enhances the expression of profibrotic genes through upregulation of the TGF-? receptor on hepatic stellate cells in a JNK-dependent manner |pdf=|usr=}}{{25210118 }} gab.com Text IL-17A enhances the expression of profibrotic genes through upregulation of the TGF- receptor on hepatic stellate cells in a JNK-dependent manner JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25210118 #FOAvip Activation of hepatic stellate cells (HSCs) is a key event in the initiation of liver fibrosis, characterized by enhanced extracellular matrix production and altered degradation. Activation of HSCs can be modulated by cytokines produced by immune cells. Recent reports have implicated the proinflammatory cytokine IL-17A in liver fibrosis progression. We hypothesized that IL-17A may enhance activation of HSCs and induction of the fibrogenic signals in these cells. The human HSC line LX2 and primary human HSCs were stimulated with increasing doses of IL-17A and compared with TGF-?- and PBS-treated cells as positive and negative controls, respectively. IL-17A alone did not induce activation of HSCs. However, IL-17A sensitized HSCs to the action of suboptimal doses of TGF-? as confirmed by strong induction of ?-smooth muscle actin, collagen type I (COL1A1), and tissue inhibitor of matrix metalloproteinase I gene expression and protein production. IL-17A specifically upregulated the cell surface expression of TGF-?RII following stimulation. Pretreatment of HSCs with IL-17A enhanced signaling through TGF-?RII as observed by increased phosphorylation of SMAD2/3 in response to stimulation with suboptimal doses of TGF-?. This enhanced TGF-? response of HSCs induced by IL-17A was JNK-dependent. Our results suggest a novel profibrotic function for IL-17A by enhancing the response of HSCs to TGF-? through activation of the JNK pathway. IL-17A acts through upregulation and stabilization of TGF-?RII, leading to increased SMAD2/3 signaling. These findings represent a novel example of cooperative signaling between an immune cytokine and a fibrogenic receptor. Twit Text FOAVip IL-17A enhances the expression of profibrotic genes through upregulation of the TGF- receptor on hepatic stellate cells in a JNK-dependent manner ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25210118 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25210118 #FOAvip English Wikipedia <ref>{{Cite pmid|25210118 }}</ref> IL-17A enhances the expression of profibrotic genes through upregulation of the TGF-? receptor on hepatic stellate cells in a JNK-dependent manner #MMPMID25210118 Fabre T ; Kared H ; Friedman SL ; Shoukry NH J Immunol 2014[Oct]; 193 (8 ): 3925-33 PMID25210118 show ga Activation of hepatic stellate cells (HSCs) is a key event in the initiation of liver fibrosis, characterized by enhanced extracellular matrix production and altered degradation. Activation of HSCs can be modulated by cytokines produced by immune cells. Recent reports have implicated the proinflammatory cytokine IL-17A in liver fibrosis progression. We hypothesized that IL-17A may enhance activation of HSCs and induction of the fibrogenic signals in these cells. The human HSC line LX2 and primary human HSCs were stimulated with increasing doses of IL-17A and compared with TGF-?- and PBS-treated cells as positive and negative controls, respectively. IL-17A alone did not induce activation of HSCs. However, IL-17A sensitized HSCs to the action of suboptimal doses of TGF-? as confirmed by strong induction of ?-smooth muscle actin, collagen type I (COL1A1), and tissue inhibitor of matrix metalloproteinase I gene expression and protein production. IL-17A specifically upregulated the cell surface expression of TGF-?RII following stimulation. Pretreatment of HSCs with IL-17A enhanced signaling through TGF-?RII as observed by increased phosphorylation of SMAD2/3 in response to stimulation with suboptimal doses of TGF-?. This enhanced TGF-? response of HSCs induced by IL-17A was JNK-dependent. Our results suggest a novel profibrotic function for IL-17A by enhancing the response of HSCs to TGF-? through activation of the JNK pathway. IL-17A acts through upregulation and stabilization of TGF-?RII, leading to increased SMAD2/3 signaling. These findings represent a novel example of cooperative signaling between an immune cytokine and a fibrogenic receptor. |*Gene Expression Regulation [MESH] |Actins/biosynthesis [MESH] |Cell Line [MESH] |Collagen Type I, alpha 1 Chain [MESH] |Collagen Type I/biosynthesis [MESH] |Hepatic Stellate Cells/*metabolism/pathology [MESH] |Humans [MESH] |Interleukin-17/pharmacology/*physiology [MESH] |JNK Mitogen-Activated Protein Kinases/*immunology [MESH] |Liver Cirrhosis/*genetics/immunology [MESH] |Liver/cytology/pathology [MESH] |Phosphorylation [MESH] |Protein Serine-Threonine Kinases/biosynthesis [MESH] |Receptor, Transforming Growth Factor-beta Type II [MESH] |Receptors, Transforming Growth Factor beta/biosynthesis/*genetics [MESH] |Signal Transduction/immunology [MESH] |Smad2 Protein/metabolism [MESH] |Smad3 Protein/metabolism [MESH] |Tissue Inhibitor of Metalloproteinase-1/biosynthesis [MESH] |Transforming Growth Factor beta/*pharmacology [MESH]IL-17A enhances the expression of profibrotic genes through upregulati(epmc).pdf DeepDyve Pubget Overpricing