Myocyte-specific enhancer factor 2C: a novel target gene of miR-214-3p in suppressing angiotensin II-induced cardiomyocyte hypertrophy

• Published in: Scientific reports Vol. 6; no. 1; p. 36146
• Main Authors: Tang, Chun-Mei, Liu, Fang-zhou, Zhu, Jie-Ning, Fu, Yong-Heng, Lin, Qiu-Xiong, Deng, Chun-Yu, Hu, Zhi-Qin, Yang, Hui, Zheng, Xi-Long, Cheng, Jian-Ding, Wu, Shu-Lin, Shan, Zhi-Xin
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 31.10.2016; Nature Publishing Group
• Subjects: 13; 13/1; 38/77; 38/79; 38/89; 42; 631/337/384/331; 64; 64/60; 692/4019/592/1540; 82; 82/80; 96; Angiotensin; Angiotensin II; Aorta; Atrial natriuretic peptide; Cardiomyocytes; Cell size; Chromosome 3; Heart; Heart diseases; Humanities and Social Sciences; Hypertrophy; miRNA; multidisciplinary; Myocardium; Myosin; Neonates; Rodents; Science; siRNA; Ventricle
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/srep36146

The role of microRNA-214-3p (miR-214-3p) in cardiac hypertrophy was not well illustrated. The present study aimed to investigate the expression and potential target of miR-214-3p in angiotensin II (Ang-II)-induced mouse cardiac hypertrophy. In mice with either Ang-II infusion or transverse aortic constriction (TAC) model, miR-214-3p expression was markedly decreased in the hypertrophic myocardium. Down-regulation of miR-214-3p was observed in the myocardium of patients with cardiac hypertrophy. Expression of miR-214-3p was upregulated in Ang-II-induced hypertrophic neonatal mouse ventricular cardiomyocytes. Cardiac hypertrophy was attenuated in Ang-II-infused mice by tail vein injection of miR-214-3p. Moreover, miR-214-3p inhibited the expression of atrial natriuretic peptide (ANP) and β-myosin heavy chain (MHC) in Ang-II-treated mouse cardiomyocytes in vitro . Myocyte-specific enhancer factor 2C (MEF2C), which was increased in Ang-II-induced hypertrophic mouse myocardium and cardiomyocytes, was identified as a target gene of miR-214-3p. Functionally, miR-214-3p mimic, consistent with MEF2C siRNA, inhibited cell size increase and protein expression of ANP and β-MHC in Ang-II-treated mouse cardiomyocytes. The NF-κB signal pathway was verified to mediate Ang-II-induced miR-214-3p expression in cardiomyocytes. Taken together, our results revealed that MEF2C is a novel target of miR-214-3p, and attenuation of miR-214-3p expression may contribute to MEF2Cexpressionin cardiac hypertrophy.