Epithelial-mesenchymal transition of intrahepatic biliary epithelial cells

赵礼金; 杨日高; 程龙; 王麦建; 江艳; 余德刚; 周廷梅; 王曙光

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Epithelial-mesenchymal transition of intrahepatic biliary epithelial cells

更新时间：2026-01-09

- Epithelial-mesenchymal transition of intrahepatic biliary epithelial cells
- Journal of Army Medical University Vol. 32, Issue 3, Pages: 214-219(2010)
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  CLC： R-33;R575.702;R394.3
- Published：2010
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赵礼金,杨日高,程龙,王麦建,江艳,余德刚,周廷梅,王曙光.肝内胆管上皮细胞上皮-间叶转化的实验研究[J].陆军军医大学学报(原第三军医大学学报),2010,32(03):214-219.

　Zhao Lijin,Yang Rigao,Cheng Long,Wang Maijian,Jiang Yan,Yu Degang,Zhou Tingmei,Wang Shuguang.Epithelial-mesenchymal transition of intrahepatic biliary epithelial cells[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(03):214-219.
赵礼金,杨日高,程龙,王麦建,江艳,余德刚,周廷梅,王曙光.肝内胆管上皮细胞上皮-间叶转化的实验研究[J].陆军军医大学学报(原第三军医大学学报),2010,32(03):214-219. DOI：

　Zhao Lijin,Yang Rigao,Cheng Long,Wang Maijian,Jiang Yan,Yu Degang,Zhou Tingmei,Wang Shuguang.Epithelial-mesenchymal transition of intrahepatic biliary epithelial cells[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(03):214-219. DOI：

摘要

目的观察人肝内胆管上皮细胞（human intrahepatic biliary epithelial cells，HIBEpiC）上皮-间叶转化（epithelial-mesenchymal transitions

EMT）现象，探讨EMT在胆管周围纤维化中的作用及其可能的分子机制。方法 HIBEpiC用脂多糖（lipopolysaccharide，LPS）处理48、72 h后，用PCR及Western blot技术检测E-cadherin、S100A4和α-SMA的表达，以及与EMT信号通路相关的TGF-β1的表达；同时用紫杉醇、siRNA smad2/3阻断TGF-β1的作用，探讨TGF-β1/smad2/3信号通路在HIBEpiC发生EMT时的可能作用。结果 HIBEpiC经LPS处理后，TGF-β1 mRNA表达于48 h达到高峰，72 h后开始下降，但维持较高水平（P0.01，P0.05）；EMT标志物E-cadherin mRNA和蛋白表达随培养时间的延长逐渐降低（P0.01），而S100A4、α-SMA mRNA及蛋白表达明显上调（P0.01，P0.05）。紫杉醇可使HIBEpiC中LPS所诱导的TGF-β1、Smad2/Smad3 mRNA表达明显下降，特别是在48 h最明显（P0.01）。用siRNA技术可使Smad2/3 mRNA及蛋白表达明显下调（P0.01），同时可使与HIBEpiC共培养EMT标志物E-cadherin mRNA及蛋白质表达上调（P0.01，P0.05），S100A4和α-SMA表达明显下调（P0.01）。结论 LPS可诱导HIBEpiC中TGF-β1的表达，使胆管上皮细胞发生EMT，抑制TGF-β1或Smad2/3，可使EMT发生逆转，提示TGF-β1或Smad2/3可能成为预防胆道周围纤维化的一个潜在靶点。

Abstract

Objective To observe the epithelial-mesenchymal transition (EMT）of human intrahepatic biliary epithelial cells (HIBEpiC) and to study its role in bile duct fibrosis and its molecular mechanism. Methods Expressions of E-cadherin

S100A4

α-SMA

and EMT signal-related TGF-β1 in HIBEpiC were detected by RT-PCR and Western blotting 48 and 72 h after treatment of HIBEpiC with lipopolysaccharide (LPS). The effect of TGF-β1 was blocked with paclitaxel and siRNA smad2/3. The role of TGF-β1/ smad2/3 signal pathway in the occurrence of EMT in HIBEpiC was studied. Results The expression of TGF-β1 mRNA reached its peak and began to decrease 48 and 72 h

respectively

after treatment of HIBEpiC with LPS

and still maintained a rather high level (P0.01

0.05). The expression level of EMT marker

E-cadherin mRNA and TGF-β1 decreased with the prolongation of culture time ( P0.01) while the expression of S100A4

α-SMA mRNA and TGF-β1 significantly increased （P0.01，0.05）

suggesting that paclitaxel can down-regulate the LPS-induced expression of TGF-β1

Smad2 and Smad3 mRNA. siRNA could also down-regulate the LPS-induced expression of Smad2/3 mRNA

S100A4

α-SMA and TGF-β1 while up-regulate the expression of E-cadherin and TGF-β1 in HIBEpiC (P0.01)

indicating that EMT can be reversed. Conclusion LPS can induce expression of TGF-β1 in HIBEpiC

resulting in EMT in biliary epithelial cells

and reverse EMT by inhibiting TGF-β1 or Smad2/3

which may be a potential target for the prevention and treatment of biliary fibrosis.

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