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目的:探讨程序性细胞死亡分子5(PDCD5)在心肌肥厚发生发展过程中的作用及机制。方法:腹主动脉缩窄术(AAC)建立大鼠心肌肥厚病理模型;苯肾上腺素(PE)刺激分离培养的乳鼠心肌细胞肥大;RT-PCR和蛋白印迹实验分别检测mRNA及蛋白表达;含PDCD5 cD NA腺病毒或PDCD5 shRNA腺病毒转染心肌细胞以过表达或敲低PDCD5;萤光素酶报告基因系统及
Objective: To investigate the role and mechanism of PDCD5 in the development of cardiac hypertrophy. Methods: A rat model of myocardial hypertrophy was established by abdominal aortic constriction (AAC). Phenylephrine (PE) stimulated cardiomyocyte hypertrophy in cultured neonatal rat cardiomyocytes. RT-PCR and Western blotting were used to detect mRNA and protein expression. PDCD5 cD NA adenovirus or PDCD5 shRNA adenovirus transfected cardiomyocytes to overexpress or knock down PDCD5; luciferase reporter system and