泛素特异性蛋白酶2促进心肌肥厚发生和发展的作用

Role of ubiquitin specific protease 2 in promoting the development of myocardial hypertrophy

目的探讨泛素特异性蛋白酶2(ubiquitin specific protease 2,USP2)在心肌肥厚发生和发展中的作用。方法使用荧光定量反转录聚合酶链反应(quantitative reverse transcription polymerase chain reaction,qRT-PCR)和Western blot检测异丙肾上腺素(isoproterenol,ISO)诱导的小鼠心肌肥厚模型中USP2的表达改变;腺病毒介导的RNA干扰技术干扰乳大鼠心肌细胞USP2的表达。使用Image J软件分析USP2对心肌细胞大小的影响,qRT-PCR检测USP2对心肌肥厚相关基因心钠素(atriopeptin,ANP),肌球蛋白重链7(myosin heavychain 7,MYH7)和脑钠肽(brain natriuretic peptide,BNP)转录水平的影响。结果ISO诱导的小鼠心脏组织中ANP、BNP及MYH7的表达上调,说明成功构建心肌肥厚小鼠模型。USP2的m RNA和蛋白在心肌肥厚的心脏组织中表达增加;干扰USP2可以降低乳大鼠心肌细胞的面积,并抑制ANP、BNP及MYH7的表达。结论USP2可以促进心肌肥厚的发生和发展。

Objectives To investigating the role of ubiquitin specific protease 2(USP2)in the development of myocar-dial hypertrophy.MethodsThe change of USP2 in isoproterenol(ISO)-induced myocardial hypertrophy model inmice was detected by fluorescence quantitative reverse transcription polymerase chain reaction(qRT-PCR)andWestern Blot.Adenovirus mediated RNA interference blunted the expression of USP2 in neonatal rat cardiac myocytes.Image J software was used to analyze the effect of USP2 on the size of cardiac myocytes and fluorescence qRT-PCR wasused to detect the effect of USP2 on the transcriptional levels of myocardial hypertrophy marker genes atriopeptin(ANP),brain natriuretic peptide(BNP)and myosin heavy chain 7(MYH7).ResultsThe expressions of ANP,BNP and MYH7 in ISO-induced mouse heart tissues were significantly up-regulated,indicating that mouse models ofmyocardial hypertrophy was successfully constructed.mRNA and protein expression of USP2 increased in cardiactissue with cardiac hypertrophy.Interference with USP2 reduced the size of neonatal rat cardiac myocytes and inhibitedthe expression of ANP,BNP and MYH7.ConclusionsUSP2 can promote myocardial hypertrophy.