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学科主题临床医学
MicroRNA-214 Mediates Isoproterenol-induced Proliferation and Collagen Synthesis in Cardiac Fibroblasts
Sun, Min; Yu, Haiyi; Zhang, Youyi; Li, Zijian1; Gao, Wei
刊名SCIENTIFIC REPORTS
2015-12-22
DOI10.1038/srep18351
5
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
资助者National Basic Research Program of China ; National Natural Science Foundation of China ; Research Fund for the Doctoral Program of Higher Education ; National Basic Research Program of China ; National Natural Science Foundation of China ; Research Fund for the Doctoral Program of Higher Education
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]HEART-FAILURE ; MYOCARDIAL FIBROSIS ; PANCREATIC-CANCER ; CELLS ; EXPRESSION ; MIR-214 ; GROWTH ; OVEREXPRESSION ; HYPERTROPHY ; PROTECTS
英文摘要

The action of beta-adrenergic receptors (beta-ARs) induces cardiac fibroblast (CF) proliferation and collagen synthesis and is a major source of the cardiac fibrosis caused by various diseases. Recently, microRNA-214 (miR-214) was found to play an important role in the pathogenesis of cardiac remodelling. In the present study, we examined the role and the underlying mechanism of miR-214 in isoproterenol (ISO, a beta-AR agonist)-induced CF proliferation and collagen synthesis. The expression of miR-214 was increased in both ISO-mediated fibrotic heart tissue and fibroblasts. Downregulation of miR-214 by antagonists attenuated the proliferation and collagen synthesis in ISO-treated CFs. Using bioinformatics analysis and luciferase assays, mitofusin2 (Mfn2), a critical regulator of cell proliferation and tissue fibrosis, was identified as a direct target gene of miR-214; this result was confirmed by western blot analysis. Additionally, corresponding to the upregulation of miR-214, the expression of Mfn2 was downregulated in the fibrotic heart and fibroblasts. Furthermore, the downregulation of miR-214 inhibited the activation of ERK1/2 MAPK signalling induced by ISO treatment. In conclusion, our study demonstrated that miR-214 mediates CF proliferation and collagen synthesis via inhibition of Mfn2 and activation of ERK1/2 MAPK signalling, which provides a new explanation for the mechanism of beta-AR activation-induced cardiac fibrosis.

语种英语
所属项目编号2014CBA02000 ; 81270157 ; 81370317 ; 81471893 ; 91539123 ; 81100164 ; 20110001120015
资助者National Basic Research Program of China ; National Natural Science Foundation of China ; Research Fund for the Doctoral Program of Higher Education ; National Basic Research Program of China ; National Natural Science Foundation of China ; Research Fund for the Doctoral Program of Higher Education
WOS记录号WOS:000367034700001
引用统计
被引频次:17[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/67165
专题北京大学第三临床医学院_心血管内科
作者单位1.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China
2.Peking Univ, Hosp 3, Dept Cardiol, Beijing 100191, Peoples R China
3.Minist Hlth, Key Lab Cardiovasc Mol Biol & Regulatory Peptides, Beijing 100191, Peoples R China
4.Beijing Key Lab Cardiovasc Receptors Res Beijing, Beijing, Peoples R China
推荐引用方式
GB/T 7714
Sun, Min,Yu, Haiyi,Zhang, Youyi,et al. MicroRNA-214 Mediates Isoproterenol-induced Proliferation and Collagen Synthesis in Cardiac Fibroblasts[J]. SCIENTIFIC REPORTS,2015,5.
APA Sun, Min,Yu, Haiyi,Zhang, Youyi,Li, Zijian,&Gao, Wei.(2015).MicroRNA-214 Mediates Isoproterenol-induced Proliferation and Collagen Synthesis in Cardiac Fibroblasts.SCIENTIFIC REPORTS,5.
MLA Sun, Min,et al."MicroRNA-214 Mediates Isoproterenol-induced Proliferation and Collagen Synthesis in Cardiac Fibroblasts".SCIENTIFIC REPORTS 5(2015).
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