Amniotic epithelial cell–derived cholangiocytes in experimental cholestatic ductal hyperplasia

摘要: AIM Bile duct paucity, ductopenia, is a feature of end-stage chronic cholangiopathies such as primary biliary cirrhosis. The limited proliferative ability cholangiocytes after specific injury thought to be the principal cause although detailed mechanisms involved are unclear. It has been reported that human amniotic epithelial cells (AEC) express differentiation markers hepatic parenchymal cells, suggesting resemblance AEC progenitor cells. aim present study was develop mouse model experimental cholestasis assess capability trans-differentiate into cholangiocytes. METHODS Enhanced green fluorescent protein (EGFP)-transgenic C57BL/6 pregnant female mice were used source AEC. At 11.5 gestational days, 1 x 10(5) isolated from EGFP-transgenic embryos and transferred mice. Chronic induced by 0.1%alpha-naphthylisothiocyanate (ANIT) feeding immediately transfer proliferation in livers assessed morphologically immunohistochemically (cytokeratin 7; CK7). activity also quantified proliferating cell nuclear antigen (PCNA) expression. EGFP confirmed laser microscopy immunofluorescent staining for EGFP. Also, Notch2 Hes1 expression evaluated examine roles this process. RESULTS Marked observed ANIT-fed quantitative CK7 (3-4 fold vs control) PCNA (11-20 staining. double positive interlobular bile ducts AEC-transferred recipients. Positivity further Moreover, both model. CONCLUSIONS Significant ductular EGFP-positive able contribute repopulating under cholestasis, might candidate stem administration future clinical applications re-model ducts.