LncRNA Meg8 suppresses activation of hepatic stellate cells and epithelial-mesenchymal transition of hepatocytes via the Notch pathway

被引:34
|
作者
Chen, Ting [1 ]
Lin, Huajiang [2 ]
Chen, Xun [3 ]
Li, Guantong [2 ]
Zhao, Yanmian [1 ]
Zheng, Lina [1 ]
Shi, Zhemin [1 ]
Zhang, Kun [1 ]
Hong, Wei [1 ]
Han, Tao [2 ]
机构
[1] Tianjin Med Univ, Dept Histol & Embryol,Publ Hlth Minist, Sch Basic Med Sci,Tianjin Key Lab Artificial Cell, Dept Hepatol & Gastroenterol,Cent Clin Coll 3, Tianjin, Peoples R China
[2] Tianjin Med Univ, Cent Clin Coll 3, Dept Hepatol & Gastroenterol,Publ Hlth Minist, Tianjin Key Lab Artificial Cells,Artificial Cell, Tianjin, Peoples R China
[3] Zhengzhou Univ, Henan Canc Hosp, Dept Hepatopancreatobiliary Surg, Affiliated Tumor Hosp, Zhengzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
Liver fibrosis; lncRNA; HSCs; EMT; Notch; LIVER FIBROSIS;
D O I
10.1016/j.bbrc.2019.11.015
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Long non-coding RNAs (lncRNAs) play an important role in various physiological and pathological processes. However, the biological role of lncRNA Meg8 in liver fibrosis is largely unknown. In this study, we found that Meg8 was over-expressed in activated hepatic stellate cells (HSCs), injured hepatocytes (HCs) and fibrotic livers. Furthermore, we revealed that Meg8 suppressed the expression of the pro-fibrogenic and proliferation genes in activated HSCs. In addition, silencing Meg8 significantly inhibited the expression of the epithelial markers, while noticeably promoted the expression of the mesenchymal markers in primary HCs and AML12 cells. Mechanistically, we demonstrated that Meg8 suppressed HSCs activation and epithelial-mesenchymal transition (EMT) of HCs through inhibiting the Notch pathway. In conclusion, our findings indicate that Meg8 may serve as a novel protective molecule and a potential therapeutic target of liver fibrosis. (C) 2019 Elsevier Inc. All rights reserved.
引用
收藏
页码:921 / 927
页数:7
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