科研成果详情

题名MicroRNA-24 regulates cardiac fibrosis after myocardial infarction
作者
发表日期2012-09
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
ISSN1582-1838
EISSN1582-4934
卷号16期号:9页码:2150-2160
DOI10.1111/j.1582-4934.2012.01523.x
页数11
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 ; SCOPUS
URL查看原文
PubMed ID22260784
SCOPUSEID2-s2.0-84865439215
通讯作者地址[Zheng, Zhe]Department of Cardiac Surgery,Cardiovascular Institute and Fu Wai Hospital,167 Beilishi Road,China
Scopus学科分类Molecular Medicine;Cell Biology
TOP期刊TOP期刊
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.State Key Laboratory of Translational Cardiovascular Medicine,Fuwai Hospital and Cardiovascular Institute,Chinese Academy of Medical Sciences, Peking Union Medical College,China;
2.Department of Surgery,Fuwai Hospital and Cardiovascular Institute,Chinese Academy of Medical Sciences, Peking Union Medical College,China;
3.Research Center for Cardiac Regenerative Medicine,Ministry of Health,China;
4.Department of Thoracic and Cardiovascular Surgery,The First Affiliated Hospital of Wenzhou Medical College,China;
5.Medical College,Xiamen University,China
第一作者单位附属第一医院
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.

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