miR-130a-3p靶向TRIM37蛋白缓解H2O2诱导的心肌损伤  

miR-130a-3p Alleviates H2O2-induced Myocardial Injury through Targeting TRIM37

作　　者：许德星 王伟 张静怡 万发银 戴若竹[1] Xu Dexing;Wang Wei;Zhang Jinyi(Department of Cardiology,Quanzhou First Hospital of Fujian Province,(Quanzhou First Hospital Affiliated to Fujian Medical University),Quanzhou 362000,China)

机构地区：[1]福建省泉州市第一医院(福建医科大学附属泉州第一医院)心内科,泉州362000

出　　处：《华中科技大学学报（医学版）》2021年第1期14-20,共7页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong

基　　金：福建省自然科学基金资助项目(No.2018J01202)。

摘　　要：目的研究微小RNA-130a-3p(miR-130a-3p)在H2O2损伤的HL-1细胞中的作用及其机制。方法建立H2O2诱导的HL-1心肌细胞氧化应激损伤模型,miR-130a-3p模拟物或TRIM37过表达载体被单独/共转染至H2O2诱导的HL-1细胞。荧光定量PCR检测miR-130a-3p水平,Western blot检测TRIM37表达;双荧光素酶报告基因实验确定miR-130a-3p和TRIM37的靶向关系。CCK8法检测HL-1细胞活力;TUNEL染色检测HL-1细胞凋亡;比色法检测细胞培养上清中乳酸脱氢酶(LDH)的含量;Western blot检测凋亡相关蛋白的表达。结果H2O2刺激后HL-1细胞miR-130a-3p表达下调,TRIM37表达上调,miR-130a-3p过表达可抑制H2O2诱导的HL-1细胞活力下降,抑制细胞凋亡,减少LDH释放量。starBase网站预测和双荧光素酶报告基因实验结果证实了TRIM37是miR-130a-3p的下游靶点。miR-130a-3p上调可抑制TRIM37的表达。同时,TRIM37过表达逆转了miR-130a-3p对H2O2诱导的心肌细胞损伤的作用,降低了细胞活力,增加了LDH释放,促进了细胞凋亡。结论miR-130a-3p可通过抑制TRIM37表达从而减轻H2O2诱导的心肌损伤。Objective To determine the effects and underlying mechanism of microRNA-130 a-3 p(miR-130 a-3 p)in H2O2-injuried HL-1 cells.Methods Oxidative stress injury model of HL-1 cardiomyocytes was established by treatment with H2O2.miR-130 a-3 p mimics or TRIM37 overexpression vector was separately transfected/co-transfected into H2O2-induced HL-1 cells.qPCR assay was applied to detect miR-130 a-3 p levels and Western blotting analysis was adopted to detect TRIM37 expression.Dual luciferase reporter assay determined the targeting relationship between miR-130 a-3 p and TRIM37.HL-1 cell viability was assessed by CCK-8 assay,and HL-1 cell apoptosis evaluated using TUNEL staining.Besides,the content of lactate dehydrogenase(LDH)in the cell supernatant was detected using the biochemical kit.In addition,levels of apoptosis-related proteins were determined by Western blotting.Results H2O2stimulation reduced miR-130 a-3 p expression and enhanced TRIM37 expression in HL-1 cells.Overexpressed miR-130 a-3 p improved the viability of H2O2-injuired HL-1 cells,suppressed cell apoptosis and reduced LDH release.StarBase website predicted and dual luciferase reporter assay confirmed that TRIM37 was the downstream target of miR-130 a-3 p.Upregulation of miR-130 a-3 p restrained TRIM37 expression.Meanwhile,TRIM37 overexpression reversed the effects of miR-130 a-3 p on H2O2-induced injury of HL-1 cells,reduced cell viability,increased LDH release,and promoted cell apoptosis.Conclusion To sum up,miR-130 a-3 p may alleviate H2O2-induced myocardial injury by repressing TRIM37 expression.

关 键 词：miR-130a-3p TRIM37 心肌损伤 

分 类 号：R542.2[医药卫生—心血管疾病]