MicroRNA-24 regulates cardiac fibrosis after myocardial infarction

doi:10.1111/j.1582-4934.2012.01523.x

科研成果详情

题名	MicroRNA-24 regulates cardiac fibrosis after myocardial infarction
作者	Wang, Jue 1,2,3,4,5; Huang, Weicong1,2,5; Xu, Ruixia 1,2,3,4; Nie, Yu 1,2,3,4; Cao, Xiaoqing 1,2,3,4; Meng, Jiang 1,2,3,4; Xu, Xiuqin 1,2,3,4,6; Hu, Shengshou 1,2,3,4; Zheng, Zhe 1,2,3,4
发表期刊	JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 影响因子和分区
语种	英语
原始文献类型	Article
关键词	myocardial infarction cardiac fibrosis microRNA-24 furin TGF-ss telocyte
其他关键词	MEDIATED ANTAGOMIR EXPRESSION ; TGF-BETA ; FABRY MICE ; LENTIVIRAL VECTORS ; LATENT TGF-BETA-1 ; CELLS ; HEART ; FURIN ; HYPERTROPHY ; FIBROBLASTS
摘要	Cardiac fibrosis after myocardial infarction (MI) has been identified as a key factor in the development of heart failure. Although dysregulation of microRNA (miRNA) is involved in various pathophysiological processes in the heart, the role of miRNA in fibrosis regulation after MI is not clear. Previously we observed the correlation between fibrosis and the miR-24 expression in hypertrophic hearts, herein we assessed how miR-24 regulates fibrosis after MI. Using qRT-PCR, we showed that miR-24 was down-regulated in the MI heart; the change in miR-24 expression was closely related to extracellular matrix (ECM) remodelling. In vivo, miR-24 could improve heart function and attenuate fibrosis in the infarct border zone of the heart two weeks after MI through intramyocardial injection of Lentiviruses. Moreover, in vitro experiments suggested that up-regulation of miR-24 by synthetic miR-24 precursors could reduce fibrosis and also decrease the differentiation and migration of cardiac fibroblasts (CFs). TGF-beta (a pathological mediator of fibrotic disease) increased miR-24 expression, overexpression of miR-24 reduced TGF-beta secretion and Smad2/3 phosphorylation in CFs. By performing microarray analyses and bioinformatics analyses, we found furin to be a potential target for miR-24 in fibrosis (furin is a protease which controls latent TGF-beta activation processing). Finally, we demonstrated that protein and mRNA levels of furin were regulated by miR-24 in CFs. These findings suggest that miR-24 has a critical role in CF function and cardiac fibrosis after MI through a furinTGF-beta pathway. Thus, miR-24 may be used as a target for treatment of MI and other fibrotic heart diseases.
资助项目	Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [30872538, 81170130]; Major State Basic Research Development Program of China (973 Program)National Basic Research Program of China [2010CB529500]
出版者	WILEY
出版地	HOBOKEN
EISSN	1582-4934
卷号	16 期号:9 页码:2150-2160
DOI	10.1111/j.1582-4934.2012.01523.x
WOS类目	Cell Biology ; Medicine, Research & Experimental
WOS研究方向	Cell Biology ; Research & Experimental Medicine
WOS记录号	WOS:000307951600022
收录类别	SCIE
发表日期	2012-09
引用统计	被引频次：204[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/11552
专题	附属第一医院
通讯作者	Zheng, Zhe
作者单位	1.Fuwai Hosp, State Key Lab Translat Cardiovasc Med, Beijing 100021, Peoples R China; 2.Chinese Acad Med Sci, Peking Union Med Coll, Cardiovasc Inst, Beijing 100730, Peoples R China; 3.Fuwai Hosp, Dept Surg, Beijing, Peoples R China; 4.Minist Hlth, Res Ctr Cardiac Regenerat Med, Beijing, Peoples R China; 5.Wenzhou Med Coll, Affiliated Hosp 1, Dept Thorac & Cardiovasc Surg, Wenzhou, Peoples R China; 6.Xiamen Univ, Coll Med, Xiamen, Fujian, Peoples R China
推荐引用方式 GB/T 7714	Wang, Jue,Huang, Weicong,Xu, Ruixia,et al. MicroRNA-24 regulates cardiac fibrosis after myocardial infarction[J]. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE,2012,16(9):2150-2160.
APA	Wang, Jue., Huang, Weicong., Xu, Ruixia., Nie, Yu., Cao, Xiaoqing., ... & Zheng, Zhe. (2012). MicroRNA-24 regulates cardiac fibrosis after myocardial infarction. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 16(9), 2150-2160.
MLA	Wang, Jue,et al."MicroRNA-24 regulates cardiac fibrosis after myocardial infarction".JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 16.9(2012):2150-2160.