Pediatric research · 2014
The expression of epithelial-mesenchymal transition-related proteins in biliary epithelial cells is associated with liver fibrosis in biliary atresia.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Xiao Yongtao, Zhou Ying, Chen Yingwei, Zhou Kejun, Wen Jie, Wang Yang, Wang Jun, Cai Wei
Аннотация
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.
CONCLUSION: 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.
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.
CONCLUSION: 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.