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The mechanism of epithelial-mesenchymal transition of human intrahepatic biliary epithelial cells induced by hypoxia/hypoxic inducible factor-1α through tgf-β1 |
YANG Zaixing1, LIANG Yan2, LIU Donghong1, ZHANG Zhencheng1, LUO Wanwan1, MAO Panying1. |
1.Department of Laboratory Medicine, Taizhou First People’s Hospital, Taizhou 318020, China; 2.Department of Laboratory Diagnostics, Shanghai Changzheng Hospital, Shanghai 200003, China
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Cite this article: |
YANG Zaixing,LIANG Yan,LIU Donghong, et al. The mechanism of epithelial-mesenchymal transition of human intrahepatic biliary epithelial cells induced by hypoxia/hypoxic inducible factor-1α through tgf-β1[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2021, 51(1): 40-44.
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Abstract Objective: To investigate the role of hypoxia/hypoxic inducible factor-1α (HIF-1α) in inducing epithelial-mesenchymal transition of human intrahepatic biliary epithelial cells (HIBEC) as well as its molecular mechanisms. Methods: Under the condition of hypoxia (1% O2), HIBECs were cultured in vitro and analyzed for mobility, invasiveness and expression levels of EMT-related markers including E-cadherin and S100A4. The above-mentioned experiments were repeated with HIF-1α silenced by siRNA and transforming growth factor β1 (TGF-β1) inhibited by inhibitor LY364947. Results: Under the condition of hypoxia, in contrast to normoxia,
HIBECs showed markedly enhanced mobility and invasiveness as well as significant downregulation of E-cadherin and upregulation of S100A4. After HIF-1α silence or TGF-β1 inhibition, above-mentioned biological changes of HIBECs were significantly inhibited under hypoxia. Conclusion: Hypoxia can induce EMT of HIBECs by activating HIF-1α. TGF-β1 plays an important role in hypoxia/HIF-1α-induced EMT of HIBECs.
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