MicroRNA-29a-3p attenuates ET-1-induced hypertrophic responses in H9c2 cardiomyocytes

被引:37
作者
Li, Man [1 ]
Wang, Nan [1 ]
Zhang, Jian [1 ]
He, Hong-Peng [1 ]
Gong, Hui-Qin [1 ]
Zhang, Rui [1 ]
Song, Tie-Feng [1 ]
Zhang, Li -Nan [1 ]
Guo, Zhi-Xia [1 ]
Cao, Dong-Sun [2 ]
Zhang, Tong-Cun [1 ,2 ]
机构
[1] Tianjin Univ Sci & Technol, Coll Biotechnol, Minist Educ & Tianjin, Key Lab Ind Fermentat Microbiol, Tianjin 300457, Peoples R China
[2] Wuhan Univ Sci & Technol, Inst Biol & Med, Wuhan 430000, Peoples R China
基金
中国国家自然科学基金; 高等学校博士学科点专项科研基金;
关键词
Cardiomyocyte hypertrophy; miR-29a-3p; NFATc4; LEFT-VENTRICULAR HYPERTROPHY; CARDIAC-HYPERTROPHY; OVERLOAD; TARGET; ACTIVATION; PROTECTS; FIBROSIS; MYOCYTES; PATHWAY; MIR-29;
D O I
10.1016/j.gene.2016.03.015
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Transcription factor nuclear factor of activated T cells c4 (NFATc4) is the best-characterized target for the development of cardiac hypertrophy. Aberrant microRNA-29 (miR-29) expression is involved in the development of cardiac fibrosis and congestive heart failure. However, whether miR-29 regulates hypertrophic processes is still not clear. In this study, we investigated the potential functions of miR-29a-3p in endothelin-1 (ET-1)-induced cardiomyocyte hypertrophy. We showed that miR-29a-3p was down-regulated in ET-1-treated H9c2 cardiomyocytes. Overexpression of miR-29a-3p significantly reduced ET-1-induced hypertrophic responses in H9c2 cardiomyocytes, which was accompanied by a decrease in NFATc4 expression. miR-29a-3p targeted directly to the 3'-UTR of NFATc4 mRNA and silenced NFATc4 expression. Our results indicate that miR-29a-3p inhibits ET-1-induced cardiomyocyte hypertrophy via inhibiting NFATc4 expression. (C) 2016 Published by Elsevier B.V.
引用
收藏
页码:44 / 50
页数:7
相关论文
共 28 条
[1]   Molecular targets and regulators of cardiac hypertrophy [J].
Agrawal, Rohini ;
Agrawal, Neeraj ;
Koyani, Chintan N. ;
Singh, Randhir .
PHARMACOLOGICAL RESEARCH, 2010, 61 (04) :269-280
[2]   MicroRNAs: Target Recognition and Regulatory Functions [J].
Bartel, David P. .
CELL, 2009, 136 (02) :215-233
[3]   Role of Endothelin in the Induction of Cardiac Hypertrophy In Vitro [J].
Bupha-Intr, Tepmanas ;
Haizlip, Kaylan M. ;
Janssen, Paul M. L. .
PLOS ONE, 2012, 7 (08)
[4]   MicroRNA-145 suppresses ROS-induced Ca2+ overload of cardiomyocytes by targeting CaMKIIδ [J].
Cha, Min-Ji ;
Jang, Jin-Kyung ;
Ham, Onju ;
Song, Byeong-Wook ;
Lee, Se-Yeon ;
Lee, Chang Yeon ;
Park, Jun-Hee ;
Lee, Jiyun ;
Seo, Hyang-Hee ;
Choi, Eunhyun ;
Jeon, Woo-min ;
Hwang, Hye Jin ;
Shin, Hyun-Taek ;
Choi, Eunmi ;
Hwang, Ki-Chul .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2013, 435 (04) :720-726
[5]   MicroRNAs are aberrantly expressed in hypertrophic heart - Do they play a role in cardiac hypertrophy? [J].
Cheng, Yunhui ;
Ji, Ruirui ;
Yue, Junming ;
Yang, Jian ;
Liu, Xiaojun ;
Chen, He ;
Dean, David B. ;
Zhang, Chunxiang .
AMERICAN JOURNAL OF PATHOLOGY, 2007, 170 (06) :1831-1840
[6]   Cardiac hypertrophy: The good, the bad and the ugly [J].
Frey, N ;
Olson, EN .
ANNUAL REVIEW OF PHYSIOLOGY, 2003, 65 :45-79
[7]   MicroRNA-29 family, a crucial therapeutic target for fibrosis diseases [J].
He, Yong ;
Huang, Cheng ;
Lin, Xiang ;
Li, Jun .
BIOCHIMIE, 2013, 95 (07) :1355-1359
[8]   Regulation of cardiac hypertrophy by intracellular signalling pathways [J].
Heineke, Joerg ;
Molkentin, Jeffery D. .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2006, 7 (08) :589-600
[9]   Endothelin-1- and isoproterenol-induced differential protein expression and signaling pathway in HL-1 cardiomyocytes [J].
Hong, Hye-Min ;
Song, Eun Joo ;
Oh, Eulsik ;
Kabir, Mohammad Humayun ;
Lee, Cheolju ;
Yoo, Young Sook .
PROTEOMICS, 2011, 11 (02) :283-297
[10]   ENDOTHELIN STIMULATES MULTIPLE RESPONSES IN ISOLATED ADULT VENTRICULAR CARDIAC MYOCYTES [J].
JONES, LG ;
ROZICH, JD ;
TSUTSUI, H ;
COOPER, G .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 263 (05) :H1447-H1454