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Here, we analyzed the consequences of inactivating EGFR signaling in the liver on the regenerative response following cholestatic injury. For that, transgenic mice overexpressing a dominant negative mutant human EGFR lacking tyrosine kinase activity (\u0394EGFR) in albumin\u2010positive cells were submitted to liver damage induced by 3,5\u2010diethoxycarbonyl\u20101,4\u2010dihydrocollidine (DDC), an experimental model resembling human primary sclerosing cholangitis. Our results show an early activation of EGFR after 1\u20132\u2009days of a DDC\u2010supplemented diet, followed by a signaling switch\u2010off. Furthermore, \u0394EGFR mice showed less liver damage and a more efficient regeneration following DDC injury. Analysis of the mechanisms driving this effect revealed an enhanced activation of mitogenic\/survival signals, AKT and ERK1\/2\u2010MAPKs, and changes in cell turnover consistent with a quicker resolution of damage in response to DDC. These changes were concomitant with profound differences in the profile of intrahepatic immune cells, consisting of a shift in the M1\/M2 balance towards M2 polarity, and the Cd4\/Cd8 ratio in favor of Cd4 lymphocytes, overall supporting an immune cell switch into a pro\u2010restorative phenotype. Interestingly, \u0394EGFR livers also displayed an amplified ductular reaction, with increased expression of EPCAM and an increased number of CK19\u2010positive ductular structures in portal areas, demonstrating an overexpansion of ductular progenitor cells. In summary, our work supports the notion that hepatocyte\u2010specific EGFR activity acts as a key player in the crosstalk between parenchymal and non\u2010parenchymal hepatic cells, promoting the pro\u2010inflammatory response activated during cholestatic injury and therefore contributing to the pathogenesis of cholestatic liver disease. \u00a9 2022 The Pathological Society of Great Britain and Ireland.<\/jats:p>","DOI":"10.1002\/path.6002","type":"journal-article","created":{"date-parts":[[2022,8,17]],"date-time":"2022-08-17T11:14:23Z","timestamp":1660734863000},"page":"312-324","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Lack of EGFR catalytic activity in hepatocytes improves liver regeneration following DDC\u2010induced cholestatic injury by promoting a pro\u2010restorative inflammatory 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