MiRNA-27b对血管紧张素Ⅱ诱导肥大心肌细胞凋亡相关因子表达的影响  

Effects of miRNA-27b on expression of apoptosis related factors in hypertrophic cardiomyocytes induced by angiotensin Ⅱ

作　　者：陈运起 吴钟伟 李堪董 赵圣吉 CHEN Yunqi;WU Zhongwei;LI Kandong;ZHAO Shengji(Department of Cardiology,Hainan West Central Hospital,Danzhou 571700,China)

机构地区：[1]海南西部中心医院心血管内科,儋州571700

出　　处：《国际心血管病杂志》2023年第3期161-164,共4页International Journal of Cardiovascular Disease

基　　金：海南省自然科学基金(820RC781)。

摘　　要：目的:观察微小RNA-27b(miR-27b)对血管紧张素Ⅱ(AngⅡ)诱导肥大心肌细胞凋亡率及凋亡相关蛋白表达的影响。方法:将H9c2小鼠心肌细胞分为4组,分别为正常对照组、AngⅡ诱导组、miR-27b mimics组和阴性核苷酸组。各组细胞建模培养后分别检测心肌细胞凋亡率,Bax、Bcl-2蛋白和mi R-27b的表达,监测心肌细胞内活性氧(ROS)水平的变化以及总超氧化物歧化酶(SOD)活性。结果:免疫荧光染色可见AngⅡ诱导组心肌细胞均较正常对照组明显肥大,细胞表面积增大,而miR-27b mimics组细胞肥大明显改善(P<0.05)。与正常对照组比较,AngⅡ诱导组Bax蛋白表达上调,而Bcl-2蛋白和miR-27b表达明显下调(P<0.05)。与AngⅡ诱导组比较,miR-27b mimics组Bax蛋白表达则减少,而Bcl-2蛋白和miR-27b表达增加(P<0.05)。与正常对照组相比,AngⅡ诱导组凋亡率显著增加(P<0.01),而与AngⅡ诱导组比较,mi R-27b mimics组凋亡率明显改善(P<0.05)。AngⅡ诱导组心肌细胞ROS水平较正常对照组上升,而总SOD活性下降,2组间比较差异均有统计学意义(P<0.05或P<0.01)。与AngⅡ诱导组比较,miR-27b mimics组ROS水平下降,而总SOD活性增加(P<0.05)。结论:miR-27b可能通过调控细胞凋亡的基因转录,参与心肌细胞肥大的发生发展。Objective:To determine the effect of microRNA-27b(miR-27b)on apoptosis rate and apoptosis-related protein expression of hypertrophic cardiomyocytes induced by angiotensin Ⅱ(AngⅡ).Methods:H9c2 mouse cardiomyocytes were divided into normal control group,AngⅡ-induced group,miR-27b mimics group,and negative nucleotide group.In each group,apoptosis rate of cardiomyocytes,expressions of Bax,Bcl-2 and miR-27b,and changes of ROS level and total SOD activity were assessed after modeling and cell culture.Results:Immunofluorescence staining showed that myocardial cells were larger and cell surface area was greater in AngⅡ-induced group than those in normal control group.These features of cell hypertrophy induced by AngⅡ was significantly improved in miR-27b mimics group(P<0.05).Compared with normal control group,AngⅡ induced an up-regulation of Bax protein expression and a down-regulation of Bcl-2 protein expression and miR-27b(P<0.05),which were reversed in miR-27b mimics group(P<0.05).Similarly,compared with normal control group,apoptosis rate was increased in AngⅡ-induced group(P<0.01),which was improved in miR-27b mimics group(P<0.05).In addition,AngⅡ induced an increase in ROS level and a decrease in total SOD activity in the myocardial cells(P<0.05 and P<0.01,respectively).ROS level was lower while SOD activity was higher in miR-27b mimics group than in AngⅡ-induced group(all P<0.05).Conclusion:Our results suggest that miR-27b may participate in the development of cardiomyocyte hypertrophy by regulating gene transcription of apoptosis.

关 键 词：心肌肥大 血管紧张素Ⅱ miRNA-27b 细胞凋亡 

分 类 号：R73[医药卫生—肿瘤]