MiR-590-3p regulates proliferation, migration and collagen synthesis of cardiac fibroblast by targeting ZEB1
文献类型： 外文期刊
作者： Yuan, Xiaolong 1 ; Pan, Jinchun 1 ; Wen, Lijuan 2 ; Gong, Baoyong 1 ; Li, Jiaqi 2 ; Gao, Hongbin 1 ; Tan, Weijiang 1 ; Li 1 ;
作者机构： 1.Guangdong Lab Anim Monitoring Inst, Guangdong Prov Key Lab Lab Anim, Guangzhou 510663, Guangdong, Peoples R China
2.South China Agr Univ, Coll Anim Sci, Natl Engn Res Ctr Swine Breeding Ind, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Guangzhou 510642, Guangdong, Peoples R China
关键词： cardiac fibrosis; miR-590-3p; myocardial infarction; ZEB1
期刊名称：JOURNAL OF CELLULAR AND MOLECULAR MEDICINE （ 影响因子：5.31； 五年影响因子：5.533 ）
ISSN： 1582-1838
年卷期： 2020 年 24 卷 1 期
页码：
收录情况： SCI
摘要： Previous studies have implicated the attractive and promising role of miR-590-3p to restore the cardiac function following myocardial infarction (MI). However, the molecular mechanisms for how miR-590-3p involves in cardiac fibrosis remain largely unexplored. Using human cardiac fibroblasts (HCFs) as the cellular model, luciferase report assay, mutation, EdU assay and transwell migration assay were applied to investigate the biological effects of miR-590-3p on the proliferation, differentiation, migration and collagen synthesis of cardiac fibroblasts. We found that miR-590-3p significantly suppressed cell proliferation and migration of HCFs. The mRNA and protein expression levels of alpha-SMA, Col1A1 and Col3A were significantly decreased by miR-590-3p. Moreover, miR-590-3p directly targeted at the 3'UTR of ZEB1 to repress the translation of ZEB1. Interfering with the expression of ZEB1 significantly decreased the cell proliferation, migration activity, mRNA and protein expressions of alpha-SMA, Col1A1 and Col3A. Furthermore, the expressions of miR-590-3p and ZEB1 were identified in infarct area of MI model in pigs. Collectively, miR-590-3p suppresses the cell proliferation, differentiation, migration and collagen synthesis of cardiac fibroblasts by targeting ZEB1. These works will provide useful biological information for future studies on potential roles of miR-590-3p as the therapeutic target to recover cardiac function following MI.
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