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.
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.
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Xiao, Y., Zhou, Y., Chen, Y. et al. The expression of epithelial–mesenchymal transition–related proteins in biliary epithelial cells is associated with liver fibrosis in biliary atresia. Pediatr Res 77, 310–315 (2015). https://doi.org/10.1038/pr.2014.181
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DOI: https://doi.org/10.1038/pr.2014.181
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