Targeting myocyte-specific enhancer factor 2D contributes to the suppression of cardiac hypertrophic growth by miR-92b-3p in mice
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Zhi-Qin Hu1,2,*, Jian-Fang Luo1,2,*, Xue-Ju Yu1,2,*, Jie-Ning Zhu1,2, Lei Huang3, Jing Yang1,4, Yong-Heng Fu1,2, Tao Li2, Yu-Mei Xue1,2, Ying-Qing Feng1,2 and Zhi-Xin Shan1,2
1Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Clinical Pharmacology, Guangzhou, China
2Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
3Department of Forensic Pathology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China
4School of Medicine, South China University of Technology, Guangzhou, China
*These authors have contributed equally to this work
Ying-Qing Feng, email: [email protected]
Zhi-Xin Shan, email: [email protected]
Keywords: microRNA-92b-3p, cardiac hypertrophy, cardiomyocyte, MEF2D
Received: June 10, 2017 Accepted: July 30, 2017 Published: September 08, 2017
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.
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