DJ-1蛋白在去氧肾上腺素诱导的心肌细胞肥厚中的作用

Role of DJ-1 in phenylephrine-induced cardiomyocyte hypertrophy

目的探讨DJ-1对去氧肾上腺素(phenylephrine,PE)诱导的心肌细胞肥厚的调控作用。方法应用PE诱导乳鼠导致心肌细胞肥厚;通过Western blot观察心肌细胞DJ-1在PE刺激下的表达量改变;通过腺病毒载体过表达DJ-1,检测过表达效率;荧光定量聚合酶链反应(polymerase chain reaction,PCR)检测心肌肥厚标志物心房利钠肽(atrial natriuretic peptide,ANP)和B型利钠肽(B type-natriuretic peptide,BNP)mRNA表达水平改变;显微镜观察心肌细胞面积改变。结果在PE诱导的心肌细胞肥厚过程中,DJ-1表达水平下调;PE可诱导ANP和BNP表达水平升高,心肌细胞面积增加;过表达DJ-1则显著抑制ANP和BNP的上调,减少心肌细胞面积的增大。结论 DJ-1可抑制PE诱导的心肌细胞肥厚。

Objectives To study how D J-1 modulates phenylephrine （PE）-induced cardiomyocyte hypertrophy.Methods In our in vitro study,PE was applied to induce cardiomyocyte hypertrophy in neonate rat.The alteration of protein expression of DJ-1 under PE stimuli was determined by using Western blot.Overexpression of DJ-1 was achieved by adenovirus transfection.The overexpression of D J-1 was confirmed by Western blot.The mRNA levels of hypertrophic biomarkers atrial natriuretic peptide （ANP） and B type natriuretic peptide （BNP） were detected by fluorescent quantitation polymerase chain reaction （FQ-PCR）.The surface area of cardiomyocytes was quantified.Results DJ-1 protein expression declined during the process of PE-induced cardiomyocyte hypertrophy.PE significantly increased the mRNA levels of ANP and BNP as well as cell surface area,an effect that was ameliorated by the overexpression of DJ-1.Conclusions D J-1 can inhibit PE-induced cardiomyocyte hypertrophy.