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10.1002/hep.28382 http://scihub22266oqcxt.onion/10.1002/hep.28382 C4764460!4764460 !26645994     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26645994 &cmd=llinks): Failed to open stream: HTTP request failed! 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Macrophage recruitment by fibrocystin-defective biliary epithelial cells promotes portal fibrosis in congenital hepatic fibrosis |pdf=|usr=}}{{26645994 }} gab.com Text Macrophage recruitment by fibrocystin-defective biliary epithelial cells promotes portal fibrosis in congenital hepatic fibrosis JO: Hepatology http://www.kidney.de/pget.php?&tw=1&pmid=26645994 #FOAvip Congenital hepatic fibrosis (CHF) is a disease of the biliary epithelium characterized by bile duct changes resembling ductal plate malformations and by progressive peribiliary fibrosis, in the absence of overt necroinflammation. Progressive liver fibrosis leads to portal hypertension and liver failure; however, the mechanisms leading to fibrosis in CHF remain elusive. CHF is caused by mutations in PKHD1, a gene encoding for fibrocystin, a ciliary protein expressed in cholangiocytes. Using a fibrocystin-defective (Pkhd1(del4/del4)) mouse, which is orthologous of CHF, we show that Pkhd1(del4/del4) cholangiocytes are characterized by a ?-catenin-dependent secretion of a range of chemokines, including chemokine (C-X-C motif) ligands 1, 10, and 12, which stimulate bone marrow-derived macrophage recruitment. We also show that Pkhd1(del4/del4) cholangiocytes, in turn, respond to proinflammatory cytokines released by macrophages by up-regulating ?v?6 integrin, an activator of latent local transforming growth factor-?1. While the macrophage infiltrate is initially dominated by the M1 phenotype, the profibrogenic M2 phenotype increases with disease progression, along with the number of portal myofibroblasts. Consistent with these findings, clodronate-induced macrophage depletion results in a significant reduction of portal fibrosis and portal hypertension as well as of liver cysts. CONCLUSION: Fibrosis can be initiated by an epithelial cell dysfunction, leading to low-grade inflammation, macrophage recruitment, and collagen deposition; these findings establish a new paradigm for biliary fibrosis and represent a model to understand the relationship between cell dysfunction, parainflammation, liver fibrosis, and macrophage polarization over time. Twit Text FOAVip Macrophage recruitment by fibrocystin-defective biliary epithelial cells promotes portal fibrosis in congenital hepatic fibrosis ????Hepatology http://www.kidney.de/pget.php?&tw=1&pmid=26645994 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26645994 #FOAvip English Wikipedia <ref>{{Cite pmid|26645994 }}</ref> Macrophage recruitment by fibrocystin-defective biliary epithelial cells promotes portal fibrosis in congenital hepatic fibrosis #MMPMID26645994 Locatelli L ; Cadamuro M ; Spirlė C ; Fiorotto R ; Lecchi S ; Morell CM ; Popov Y ; Scirpo R ; De Matteis M ; Amenduni M ; Pietrobattista A ; Torre G ; Schuppan D ; Fabris L ; Strazzabosco M Hepatology 2016[Mar]; 63 (3 ): 965-82 PMID26645994 show ga Congenital hepatic fibrosis (CHF) is a disease of the biliary epithelium characterized by bile duct changes resembling ductal plate malformations and by progressive peribiliary fibrosis, in the absence of overt necroinflammation. Progressive liver fibrosis leads to portal hypertension and liver failure; however, the mechanisms leading to fibrosis in CHF remain elusive. CHF is caused by mutations in PKHD1, a gene encoding for fibrocystin, a ciliary protein expressed in cholangiocytes. Using a fibrocystin-defective (Pkhd1(del4/del4)) mouse, which is orthologous of CHF, we show that Pkhd1(del4/del4) cholangiocytes are characterized by a ?-catenin-dependent secretion of a range of chemokines, including chemokine (C-X-C motif) ligands 1, 10, and 12, which stimulate bone marrow-derived macrophage recruitment. We also show that Pkhd1(del4/del4) cholangiocytes, in turn, respond to proinflammatory cytokines released by macrophages by up-regulating ?v?6 integrin, an activator of latent local transforming growth factor-?1. While the macrophage infiltrate is initially dominated by the M1 phenotype, the profibrogenic M2 phenotype increases with disease progression, along with the number of portal myofibroblasts. Consistent with these findings, clodronate-induced macrophage depletion results in a significant reduction of portal fibrosis and portal hypertension as well as of liver cysts. CONCLUSION: Fibrosis can be initiated by an epithelial cell dysfunction, leading to low-grade inflammation, macrophage recruitment, and collagen deposition; these findings establish a new paradigm for biliary fibrosis and represent a model to understand the relationship between cell dysfunction, parainflammation, liver fibrosis, and macrophage polarization over time. |Animals [MESH] |Antigens, Neoplasm/metabolism [MESH] |Chemokines/*metabolism [MESH] |Clodronic Acid [MESH] |Collagen/metabolism [MESH] |Disease Models, Animal [MESH] |Epithelial Cells/*metabolism [MESH] |Genetic Diseases, Inborn/*immunology/metabolism [MESH] |Integrins/metabolism [MESH] |Liver Cirrhosis/*immunology/metabolism [MESH] |Macrophages/*physiology [MESH] |Mice [MESH] |Myofibroblasts/physiology [MESH] |Receptors, Cell Surface/*deficiency [MESH] |Snail Family Transcription Factors [MESH] |Transcription Factors/metabolism [MESH] |Transforming Growth Factor beta1/metabolism [MESH]Macrophage recruitment by fibrocystin-defective biliary epithelial cel(epmc).pdf DeepDyve Pubget Overpricing