Knockdown of HIPK2 attenuates the pro-fibrogenic response of hepatic stellate cells induced by TGF-β1

被引：14
作者：
He, Ping [1 ]
Yu, Zu-jiang [1 ]
Sun, Chang-yu [1 ]
Jiao, Shu-jie [2 ]
Jiang, He-qing [1 ]
机构：
[1] Zhengzhou Univ, Dept Infect Dis, Affiliated Hosp 1, Zhengzhou 450000, Peoples R China
[2] Zhengzhou Univ, Dept Neurol, Affiliated Hosp 1, Zhengzhou 450000, Peoples R China
来源：
BIOMEDICINE & PHARMACOTHERAPY | 2017年 / 85卷
关键词：
Liver fibrosis; Homeodomain-interacting protein kinase 2 (HIPK2); Hepatic stellate cells (HSCs); TGF-beta 1/Smad pathway; LIVER FIBROSIS; EXTRACELLULAR-MATRIX; SIGNALING PATHWAY; TGF-BETA; EXPRESSION; PROTEIN; ACTIVATION; COLLAGEN; SMAD3; PROLIFERATION;
D O I：
10.1016/j.biopha.2016.11.066
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
Homeodomain-interacting protein kinase 2 (HIPK2), a member of HIPKs family, is considered as a key regulator in fibrosis. However, the roles of HIPK2 in hepatic stellate cells (HSCs) activation and liver fibrosis are still unclear. Therefore, in this study, we investigated the roles of HIPK2 in HSCs activation and liver fibrosis. Our results showed that HIPK2 expression was significantly up-regulated in liver fibrotic tissues and TGF-b1-treated HSCs. Knockdown of HIPK2 significantly inhibited TGF-beta 1-induced HSCs proliferation, as well as decreased the expression levels of alpha-SMA and collagen I. Furthermore, knockdown of HIPK2 attenuated the phosphorylation of Smad3 in the presence of TGF-beta 1. In conclusion, these results demonstrated that HIPK2 may function as a novel regulator to modulate HSC activation, potentially by inhibiting the TGF-beta 1/Smad3 signaling pathway. The results provide supporting evidence that HIPK2 may be a potential target for the treatment of liver fibrosis. (C) 2016 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码：575 / 581
页数：7
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