title: The expression of epithelial-mesenchymal transition-related proteins in biliary epithelial cells is associated with liver fibrosis in biliary atresia.
abstract: BACKGROUND
  The epithelial-mesenchymal transition (EMT) has been implicated as a key mechanism in the pathogenesis of liver fibrosis. The miR-200 family has been shown to inhibit EMT.
  
  
  METHODS
  Liver fibrosis levels were assessed with Masson's trichrome staining of liver samples obtained from biliary atresia (BA) patients. The expressions of cytokeratin-7 (CK-7) and α-smooth muscle actin (α-SMA) in the liver sections were detected by immunohistochemical and immunofluorescent staining. EMTs were induced by transforming growth factor (TGF)-β1 in human biliary epithelial cells (BECs) in vitro.
  
  
  RESULTS
  We showed that the EMT-related proteins CK-7 and α-SMA colocalized to the intrahepatic BECs in the liver sections of patients with BA. The level of α-SMA expression was related to liver fibrosis stage in BA. EMT in primary human intrahepatic BECs was induced by TGF-β1 in vitro. miR-200b is one member of the miR-200 family and significantly inhibited TGF-β1-mediated EMT in BECs.
  
  
  CONCLUSIONS
  Together, these data suggest that the occurrence of EMT in BECs might contribute to BA fibrosis. miR-200b significantly affects the development and progression of TGF-β1-dependent EMT and fibrosis in vitro.
authors.affiliation: 1] Department of Pediatric Surgery, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China [2] Shanghai Institute of Pediatric Research, Shanghai, China [3] Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Shanghai, China.
authors.forename: Yongtao
authors.initials: Y
authors.lastname: Xiao
authors.affiliation: 1] Department of Pediatric Surgery, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China [2] Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Shanghai, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhou
authors.affiliation: 1] Shanghai Institute of Pediatric Research, Shanghai, China [2] Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Shanghai, China.
authors.forename: Yingwei
authors.initials: Y
authors.lastname: Chen
authors.affiliation: 1] Shanghai Institute of Pediatric Research, Shanghai, China [2] Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Shanghai, China.
authors.forename: Kejun
authors.initials: K
authors.lastname: Zhou
authors.affiliation: 1] Shanghai Institute of Pediatric Research, Shanghai, China [2] Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Shanghai, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Wen
authors.affiliation: 1] Shanghai Institute of Pediatric Research, Shanghai, China [2] Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Shanghai, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.affiliation: 1] Department of Pediatric Surgery, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China [2] Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Shanghai, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.affiliation: 1] Department of Pediatric Surgery, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China [2] Shanghai Institute of Pediatric Research, Shanghai, China [3] Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Shanghai, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Cai
mesh_terms: D000199:Actins / Q000378:metabolism*; D001652:Bile Ducts / Q000166:cytology; D001656:Biliary Atresia / Q000150:complications*; D004847:Epithelial Cells / Q000378:metabolism*; D058750:Epithelial-Mesenchymal Transition / Q000502:physiology*; D005455:Fluorescent Antibody Technique; D006801:Humans; D007150:Immunohistochemistry; D053552:Keratin-7 / Q000378:metabolism*; D008103:Liver Cirrhosis / Q000209:etiology / Q000503:physiopathology*; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D053552:Keratin-7; D053773:Transforming Growth Factor beta1