NOS和PTEN在血管紧张素Ⅱ诱导心肌细胞肥大中的作用  

EFFECT OF NOS AND PTEN ON CARDIOMYOCYTE HYPERTROPHY INDUCED BY ANGIOTENSIN II

作　　者：吴扬[1] 胡亚娥[1] 

机构地区：[1]南通医学院航海医学研究所,江苏南通226001

出　　处：《中国应用生理学杂志》2005年第1期41-45,共5页Chinese Journal of Applied Physiology

基　　金：江苏省高校自然科学研究计划项目 (0 0KJB3 10 0 0 1)

摘　　要：目的 :研究NOS和PTEN在AngⅡ诱导的心肌细胞肥大中的作用及其机制。方法 :采用AngⅡ诱导新生大鼠心肌细胞肥大模型 ,应用RT PCR、Westernblot及免疫组化等方法 ,分别检测各组心肌细胞eNOS、iNOS、PTENmRNA表达和PTEN蛋白表达的变化 ,以及PTEN蛋白定位。结果 :①应用AngⅡ培养 1d的心肌细胞 ,心肌细胞蛋白质含量未见明显变化 ,但eNOSmRNA表达显著减少 ,iNOSmRNA表达显著增加。②应用AngⅡ培养 5d的心肌细胞 ,心肌细胞蛋白质含量显著增加 ;eNOSmRNA和iNOSmRNA表达未见明显变化 ;心肌细胞PTEN蛋白表达显著减少。③免疫组化结果显示 ,心肌细胞核内有棕黄色细颗粒状的免疫产物生成。结论 :NOS和PTEN参与了血管紧张素Ⅱ诱导心肌细胞肥大的发生发展过程。Aim: To investigate the effect of NOS and PTEN on the hypertrophic response induced by angiotensin II in the primary culture of neonatal rat cardiomyocytes.Methods: Total protein content of cardiomyocytes was used as the index of cardiac myocyte hypertrophy. eNOS mRNA, iNOS mRNA and PTEN mRNA expression were assessed using RT-PCR normalized with GAPDH. PTEN protein was determined by Western blot and immunohistochemistry method. Results: ① On day 1 after AngⅡ treatment, the expression of eNOS mRNA was significantly decreased whereas iNOS mRNA expression was significantly increased. The effect of AngⅡ on NOS expression was inhibited by L-arginine. ② Total protein content of cardiomyocytes increased significantly on day 5 after AngⅡ treatment, and PTEN protein expression was significantly decreased. The increased protein content and the decreased expression of PTEN protein were inhibited by L-Arg. The L-arginine effect was blocked by L-NAME(NOS inhibitor). ③ The positive immunocytochemical product of PTEN was mainly located in the nucleus of myocardiocyte. Conclusion: These results indicate that NOS and PTEN may take part in the process of cardiac myocyte hypertrophy induced by AngⅡ. The effect of L-arginine on cardiomyocytes may be mediated by NOS/NO and PTEN.

关 键 词：NOS PTEN 心肌细胞肥大 

分 类 号：R331.3[医药卫生—人体生理学]