单位：[1]Department of Clinical Laboratory, Peking University People's Hospital, Beijing, People's Republic of China.[2]State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People's Republic of China.[3]Department of Cardiovascular Surgery, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People's Republic of China.[4]Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, People's Republic of China.临床科室泌尿外科泌尿外科首都医科大学附属北京友谊医院[5]National Research Institute for Family Planning, Peking Union Medical College, Beijing, People's Republic of China.
Hypertrophic cardiomyopathy (HCM) is a serious monogenic disease characterized by cardiac hypertrophy, fibrosis, sudden cardiac death, and heart failure. Previously, we identified that miR-139-5p was down-regulated in HCM patients. However, the regulatory effects of miR-139-5p remain unclear. Thus, we investigated the role of miR-139-5p in the regulation of cardiac hypertrophy. The expression of miR-139-5p in left ventricular tissues in HCM patients and mice subjected to transverse aortic constriction (TAC) was significantly down-regulated. Knockdown of miR-139-5p expression in neonatal rat cardiomyocytes (NRCMs) induced cardiomyocyte enlargement and increased atrial natriuretic polypeptide (ANP) expression. Overexpression of miR-139-5p antagonized isoproterenol (ISO)-induced cardiomyocyte enlargement and ANP/brain natriuretic peptide (BNP) up-regulation. More importantly, we found that c-Jun expression was inhibited by miR-139-5p in NRCMs. Knockdown of c-Jun expression significantly attenuated cardiac hypertrophy induced by miR-139-5p deprivation. Our data indicated that miR-139-5p was down-regulated in the hearts of HCM patients and that it inhibited cardiac hypertrophy by targetting c-Jun expression.
基金：
National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81500236]
第一作者单位：[1]Department of Clinical Laboratory, Peking University People's Hospital, Beijing, People's Republic of China.[2]State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People's Republic of China.[*1]Department of Clinical Laboratory, Peking University People's Hospital, No. 11 Xizhimennan Street, Xicheng District, Beijing 100044, China.
共同第一作者：
通讯作者：
通讯机构：[1]Department of Clinical Laboratory, Peking University People's Hospital, Beijing, People's Republic of China.[2]State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People's Republic of China.[*1]Department of Clinical Laboratory, Peking University People's Hospital, No. 11 Xizhimennan Street, Xicheng District, Beijing 100044, China.[*2]State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 167 Beilishilu, Xicheng District, Beijing 100037, China.
推荐引用方式(GB/T 7714)：
Su Ming,Wang Shui-yun,Qiu Wei,et al.miR-139-5p inhibits isoproterenol-induced cardiac hypertrophy by targetting c-Jun[J].BIOSCIENCE REPORTS.2018,38:doi:10.1042/BSR20171430.
APA：
Su Ming,Wang Shui-yun,Qiu Wei,Li Jian-hui,Hui Ru-tai...&Wang Ji-zheng.(2018).miR-139-5p inhibits isoproterenol-induced cardiac hypertrophy by targetting c-Jun.BIOSCIENCE REPORTS,38,
MLA：
Su Ming,et al."miR-139-5p inhibits isoproterenol-induced cardiac hypertrophy by targetting c-Jun".BIOSCIENCE REPORTS 38.(2018)
