抑制真核翻译起始因子3a（eIF3a）可减弱转化生长因子-β1（TGF-β1）诱导的肝星状细胞促纤维化反应。
Knockdown of eIF3a attenuates the pro-fibrogenic response of hepatic stellate cells induced by TGF-β1.
作者信息
He P, Yu Z-J, Sun C-Y, Jiao S-J, Jiang H-Q
机构信息
The First Affiliated Hospital of Zhengzhou University Department of Infectious Diseases Zhengzhou China.
The First Affiliated Hospital of Zhengzhou University Department of Infectious Diseases Zhengzhou China
出版信息
Cell Mol Biol (Noisy-le-grand). 2016 May 30;62(6):107-11.
Activation of hepatic stellate cells (HSCs) plays an important role in the development of liver fibrosis. The eukaryotic translation initiation factor (eIF) 3a is the largest subunit of the eIF3 complex and has been involved in pulmonary fibrosis. However, the role of eIF3a in liver fibrosis remains largely unknown. Therefore, in this study, we investigated the role of eIF3a in transforming growth factor-β1 (TGF-β1)-induced HSC activation. Our results demonstrated that the expression of eIF3a was up-regulated in human liver fibrotic tissues and activated HSCs. In addition, knockdown of eIF3a suppressed TGF-β-induced HSC proliferation and the expression of α-smooth muscle actin (α-SMA) and collagen I. Furthermore, knockdown of eIF3a inhibited the expression of p-Smad3 induced by TGF-β1 in HSCs. These results suggest that eIF3a may function as a novel regulator to modulate HSC activation, potentially through inhibiting the TGF-β1/Smad3 signaling pathway.
肝星状细胞（HSCs）的激活在肝纤维化的发展过程中起重要作用。真核翻译起始因子（eIF）3a是eIF3复合体的最大亚基，并且已参与肺纤维化。然而，eIF3a在肝纤维化中的作用仍很大程度上未知。因此，在本研究中，我们调查了eIF3a在转化生长因子-β1（TGF-β1）诱导的肝星状细胞激活中的作用。我们的结果表明，eIF3a的表达在人肝纤维化组织和活化的肝星状细胞中上调。此外，敲低eIF3a可抑制TGF-β诱导的肝星状细胞增殖以及α-平滑肌肌动蛋白（α-SMA）和I型胶原的表达。此外，敲低eIF3a可抑制TGF-β1在肝星状细胞中诱导的p-Smad3的表达。这些结果表明，eIF3a可能作为一种新型调节因子来调节肝星状细胞的激活，可能是通过抑制TGF-β1/Smad3信号通路来实现的。
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