Administration of miR-92b-3p mimic attenuated angiotensin II-induced cardiac hypertrophy in mice and inhibited cardiomyocyte growth by targeting myocyte-specific enhancer factor 2D (MEF2D).
miR-92b-3p attenuates Ang-II-induced cardiac hypertrophy by targeting MEF2D, highlighting a potential novel mechanism and therapeutic target.
// Zhi-Qin Hu 1, 2, * , Jian-Fang Luo 1, 2, * , Xue-Ju Yu 1, 2, * , Jie-Ning Zhu 1, 2 , Lei Huang 3 , Jing Yang 1, 4 , Yong-Heng Fu 1, 2 , Tao Li 2 , Yu-Mei Xue 1, 2 , Ying-Qing Feng 1, 2 and Zhi-Xin Shan 1, 2 1 Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangzhou, China 2 Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China 3 Department of Forensic Pathology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China 4 School of Medicine, South China University of Technology, Guangzhou, China * These authors have contributed equally to this work Correspondence to: Ying-Qing Feng, email: fyq1819@163.com Zhi-Xin Shan, email: zhixinshan@aliyun.com Keywords: microRNA-92b-3p, cardiac hypertrophy, cardiomyocyte, MEF2D Received: June 10, 2017 Accepted: July 30, 2017 Published: September 08, 2017 ABSTRACT The role of microRNA-92b-3p (miR-92b-3p) in cardiac hypertrophy was not well illustrated. The present study aimed to investigate the expression and potential target of miR-92b-3p in angiotensin II (Ang-II)-induced mouse cardiac hypertrophy. MiR-92b-3p was markedly decreased in the myocardium of Ang-II-infused mice and of patients with cardiac hypertrophy. However, miR-92b-3p expression was revealed increased in Ang-II-induced neonatal mouse cardiomyocytes. Cardiac hypertrophy was shown attenuated in Ang-II-infused mice received tail vein injection of miR-92b-3p mimic. Moreover, miR-92b-3p inhibited the expression of atrial natriuretic peptide (ANP), skeletal muscle α-actin (ACTA1) and β-myosin heavy chain (MHC) in Ang-II-induced mouse cardiomyocytes in vitro . Myocyte-specific enhancer factor 2D (MEF2D), which was increased in Ang-II-induced mouse hypertrophic myocardium and cardiomyocytes, was identified as a target gene of miR-92b-3p. Functionally, miR-92b-3p mimic, consistent with MEF2D siRNA, inhibited cell size increase and protein expression of ANP, ACTA1 and β-MHC in Ang-II-treated mouse cardiomyocytes. Taken together, we demonstrated that MEF2D is a novel target of miR-92b-3p, and attenuation of miR-92b-3p expression may contribute to the increase of MEF2D in cardiac hypertrophy.
Hu et al. (Fri,) conducted a other in Cardiac hypertrophy. miR-92b-3p mimic vs. Control was evaluated on Cardiac hypertrophy and expression of ANP, ACTA1, and β-MHC. Administration of miR-92b-3p mimic attenuated angiotensin II-induced cardiac hypertrophy in mice and inhibited cardiomyocyte growth by targeting myocyte-specific enhancer factor 2D (MEF2D).