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10.1016/j.jhep.2016.01.010 http://scihub22266oqcxt.onion/10.1016/j.jhep.2016.01.010 C4834254!4834254 !26806818     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26806818 &cmd=llinks): Failed to open stream: HTTP request failed! 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Characterization of hepatic stellate cells, portal fibroblasts, and mesothelial cells in normal and fibrotic livers |pdf=|usr=}}{{26806818 }} gab.com Text Characterization of hepatic stellate cells, portal fibroblasts, and mesothelial cells in normal and fibrotic livers JO: J Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=26806818 #FOAvip BACKGROUND & AIMS: Contribution of hepatic stellate cells (HSCs), portal fibroblasts (PFs), and mesothelial cells (MCs) to myofibroblasts is not fully understood due to insufficient availability of markers and isolation methods. The present study aimed to isolate these cells, characterize their phenotypes, and examine their contribution to myofibroblasts in liver fibrosis. METHODS: Liver fibrosis was induced in Collagen1a1-green fluorescent protein (Col1a1(GFP)) mice by bile duct ligation (BDL), 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet, or CCl4 injections. Combining vitamin A (VitA) lipid autofluorescence and expression of GFP and glycoprotein M6a (GPM6A), we separated HSCs, PFs, and MCs from normal and fibrotic livers by fluorescence-activated cell sorting (FACS). RESULTS: Normal Col1a1(GFP) livers broadly expressed GFP in HSCs, PFs, and MCs. Isolated VitA+ HSCs expressed reelin, whereas VitA-GFP+GPM6A- PFs expressed ectonucleoside triphosphate diphosphohydrolase-2 and elastin. VitA-GFP+GPM6A+ MCs expressed keratin 19, mesothelin, and uroplakin 1b. Transforming growth factor (TGF)-?1 treatment induced the transformation of HSCs, PFs, and MCs into myofibroblasts in culture. TGF-?1 suppressed cyclin D1 mRNA expression in PFs but not in HSCs and MCs. In biliary fibrosis, PFs adjacent to the bile duct expressed ?-smooth muscle actin. FACS analysis revealed that HSCs are the major source of GFP+ myofibroblasts in the injured Col1a1(GFP) mice after DDC or CCl4 treatment. Although PFs partly contributed to GFP+ myofibroblasts in the BDL model, HSCs were still dominant source of myofibroblasts. CONCLUSION: HSCs, PFs, and MCs have distinct phenotypes, and PFs partly contribute to myofibroblasts in the portal triad in biliary fibrosis. Twit Text FOAVip Characterization of hepatic stellate cells, portal fibroblasts, and mesothelial cells in normal and fibrotic livers ????J Hepatol http://www.kidney.de/pget.php?&tw=1&pmid=26806818 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26806818 #FOAvip English Wikipedia <ref>{{Cite pmid|26806818 }}</ref> Characterization of hepatic stellate cells, portal fibroblasts, and mesothelial cells in normal and fibrotic livers #MMPMID26806818 Lua I ; Li Y ; Zagory JA ; Wang KS ; French SW ; Sévigny J ; Asahina K J Hepatol 2016[May]; 64 (5 ): 1137-1146 PMID26806818 show ga BACKGROUND & AIMS: Contribution of hepatic stellate cells (HSCs), portal fibroblasts (PFs), and mesothelial cells (MCs) to myofibroblasts is not fully understood due to insufficient availability of markers and isolation methods. The present study aimed to isolate these cells, characterize their phenotypes, and examine their contribution to myofibroblasts in liver fibrosis. METHODS: Liver fibrosis was induced in Collagen1a1-green fluorescent protein (Col1a1(GFP)) mice by bile duct ligation (BDL), 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet, or CCl4 injections. Combining vitamin A (VitA) lipid autofluorescence and expression of GFP and glycoprotein M6a (GPM6A), we separated HSCs, PFs, and MCs from normal and fibrotic livers by fluorescence-activated cell sorting (FACS). RESULTS: Normal Col1a1(GFP) livers broadly expressed GFP in HSCs, PFs, and MCs. Isolated VitA+ HSCs expressed reelin, whereas VitA-GFP+GPM6A- PFs expressed ectonucleoside triphosphate diphosphohydrolase-2 and elastin. VitA-GFP+GPM6A+ MCs expressed keratin 19, mesothelin, and uroplakin 1b. Transforming growth factor (TGF)-?1 treatment induced the transformation of HSCs, PFs, and MCs into myofibroblasts in culture. TGF-?1 suppressed cyclin D1 mRNA expression in PFs but not in HSCs and MCs. In biliary fibrosis, PFs adjacent to the bile duct expressed ?-smooth muscle actin. FACS analysis revealed that HSCs are the major source of GFP+ myofibroblasts in the injured Col1a1(GFP) mice after DDC or CCl4 treatment. Although PFs partly contributed to GFP+ myofibroblasts in the BDL model, HSCs were still dominant source of myofibroblasts. CONCLUSION: HSCs, PFs, and MCs have distinct phenotypes, and PFs partly contribute to myofibroblasts in the portal triad in biliary fibrosis. |Animals [MESH] |Cells, Cultured [MESH] |Epithelium/*pathology [MESH] |Fibroblasts/pathology [MESH] |Flow Cytometry [MESH] |Hepatic Stellate Cells/*pathology [MESH] |Liver Cirrhosis, Experimental/*pathology [MESH] |Liver/*pathology [MESH] |Mesothelin [MESH] |Mice [MESH] |Portal Vein/*pathology [MESH]Characterization of hepatic stellate cells, portal fibroblasts, and me(epmc).pdf DeepDyve Pubget Overpricing