心钠素
钙网蛋白
血管紧张素II
内科学
肌肉肥大
下调和上调
内质网
内分泌学
脑利钠肽
小RNA
心力衰竭
基因敲除
肾素-血管紧张素系统
未折叠蛋白反应
免疫印迹
转染
利钠肽
心肌细胞
医学
生物
细胞生物学
细胞凋亡
细胞培养
受体
血压
生物化学
遗传学
基因
作者
Qinxue Bao,L. Chen,J. Li,Mingyue Zhao,Si-Pei Wu,Wenchao Wu,X. Liu
出处
期刊:Cellular and Molecular Biology
日期:2017-04-29
卷期号:63 (4): 23-23
被引量:27
标识
DOI:10.14715/cmb/2017.63.4.4
摘要
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.
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