Open AccessRole of microRNA-124 in cardiomyocyte hypertrophy inducedby angiotensin II
Author(s) -
Qinxue Bao,
L. Chen,
J. Li,
Mingyue Zhao,
Si-Pei Wu,
Wenchao Wu,
X. Liu
Publication year - 2017
Publication title -
cellular and molecular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.371
H-Index - 71
eISSN - 1165-158X
pISSN - 0145-5680
DOI - 10.14715/cmb/2017.63.4.4
Subject(s) - atrial natriuretic peptide , calreticulin , angiotensin ii , medicine , muscle hypertrophy , downregulation and upregulation , endoplasmic reticulum , endocrinology , brain natriuretic peptide , microrna , heart failure , gene knockdown , renin–angiotensin system , unfolded protein response , western blot , transfection , natriuretic peptide , myocyte , biology , microbiology and biotechnology , apoptosis , cell culture , receptor , blood pressure , genetics , gene , biochemistry
Cardiac hypertrophy is a crucial predictor of heart failure and is regulated by microRNAs. MicroRNA-124 (miR-124) is regarded as a prognostic indicator for outcomes after cardiac arrest. However, whether miR-124 participates in cardiac hypertrophy remains unclear. Therefore, our study aimed to determine the role of miR-124 in angiotensin II(AngII)-induced myocardial hypertrophy and the possible mechanism. Primary cultured rat neonatal cardiomyocytes(NCMs) were transfected with miR-124 mimics or inhibitor, followed by AngII stimulation. Quantitative RT-PCR, western blot analysis and determination of cell surface area of NCMs were used to detect the hypertrophic phenotypes. We observed that miR-124 was elevated in AngII-induced hypertrophic cardiomyocytes. Cell surface area of NCMs and mRNA expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC), indicators of myocardial hypertrophy, were higher in NCMs transfected with miR-124 mimics in the presence of AngII. On the contrary, knockdown of miR-124 by its specific inhibitor could restore these courses. Furthermore, downregulation of miR-124 alleviated the increased protein level of endoplasmic reticulum (ER) stress markers 78-kDa glucose-regulated protein (Grp78) and calreticulin(CRT) in AngII-induced NCMs. In conclusion, our study shows that inhibition of miR-124 effectively suppresses AngII-induced myocardial hypertrophy, which is associated with attenuation of ER stress.