miR-155下调心肌细胞ATR1α表达改善心肌细胞肥大  

miR-155 down-regulate cardiomyocyte′s ATR1α receptor to inhibit cardiac hypertrophy

作　　者：杨勇[1] 周勇[2] 曹政[1] 吴瑞霞[1] 佟新竹 谢华强[1] 

机构地区：[1]湖北医药学院附属十堰市太和医院心血管内科,442000 [2]湖北医药学院附属十堰市太和医院肿瘤内科,442000

出　　处：《重庆医学》2015年第21期2890-2894,共5页Chongqing medicine

基　　金：湖北省十堰市科技局2012年科学技术研究与开发指导项目(ZD2012014)

摘　　要：目的研究微小RNA(miR)-155对心肌细胞肥大的影响,以及血管紧张素Ⅱ(AngⅡ)受体1α亚型(angiotensinⅡreceptor subtype 1α,ATR1α)在其中的作用。方法AngⅡ诱导体外培养大鼠心肌细胞H9C2(2-1)肥大,将miR-155模拟物(mimics)和miR-155抑制物(inhibitors)转染入心肌细胞。测量心肌细胞表面积。实验分为对照组、AngⅡ组、模拟物组、miR-155抑制物组、AngⅡ加模拟物组、AngⅡ加抑制物组。实时荧光定量PCR检测心肌细胞miR-155的表达。逆转录PCR法检测心房钠尿肽(ANP)、β-肌球蛋白重链(β-MHC)、ATR1αmRNA表达水平。Western blot法检测ATR1α蛋白表达水平。结果与AngⅡ组比较,AngⅡ加模拟物组处理可降低心肌细胞ANP、β-MHC mRNA及ATR1αmRNA和蛋白表达水平(P<0.05),心肌细胞表面积降低(P<0.05);AngⅡ加抑制物组处理ATR1αmRNA和蛋白表达水平增加(P<0.05),但ANP、β-MHC mRNA表达水平及心肌细胞表面积改变差异无统计学意义(P>0.05),仅miR-155mimics或miR-155inhibitors处理各项指标均改变差异无统计学意义(P>0.05)。结论 miR-155过表达抑制心肌细胞肥大;ATR1α可能为其负性调控作用靶点。Objective To observe the effects of microRNA-155（mi1α-155） on angiotensin Ⅱ receptor subtype 1 α（ATRla） and itrs effects on cardiomyocyte hypertrophy. Methods Angiotensin Ⅱ was used to induce cultured rat myocardial cells H9C2 （2- 1） to be cardiac hypertrophy, miR-155 mimics （mimics） and miR-155 inhibitor （inhibitors） were transfected into myocardial cells by Liposome transfection method. Myocardial cell surface were measured through Leica phase contrast microscopy image analysis software. There were four groups,including control group, Ang Ⅱ group, mimics group, miR-155 inhibitors group, Ang Ⅱ ＋ mimics group, Ang Ⅱ ＋inhibitors group. Real-time PCR was used to detect the expression of miR-155 myocardial cells. RT-PCR were used to detect atrial natriuretic peptide （ANP）, B-myosin heavy chain （β-MHC） and ATRla mRNA expression levels. Western blot assay was used to detect the expression of ATR1α protein. Results Compared with Ang Ⅱ group, the expression of ANP,β-MHC mRNA and the myocardial cell surface area were significantly lower in Ang Ⅱ ＋mimics group（P〈0.05）. The expression levels of ATRIa mRNA and protein were significantly lower （P〈0.05）. In Ang Ⅱ ＋ inhibitors group, the levels of ATR1α mRNA and protein were higher than Ang Ⅱ group （P〈0.05）, but the expression of ANP,Ⅱ＋MHC mRNA and the myocardial cell surface area have no difference all （P〉0.05）. There were no difference between control group, mimics group and inhibitors group（P〉0.05）. Conclusion miR-155 may inhibit cardiac hypertrophy through down-regulate the expression of ATR1α.

关 键 词：微RNAS 基因疗法 受体 血管紧素 1型 心肌肥大 

分 类 号：R542.2[医药卫生—心血管疾病]