mAKAPβ在AngⅡ促新生大鼠心肌细胞肥大中的作用及其机制  

Effect of mAKAPβ on AngⅡ-induced cardiac hypertrophy and its mechanism

作　　者：徐元熙[1] 侯磊[1] 李宪凯[1] 闻静[1] 魏毅东[1] 徐亚伟[1] 

机构地区：[1]同济大学附属第十人民医院心内科,上海200072

出　　处：《同济大学学报（医学版）》2013年第4期1-5,共5页Journal of Tongji University(Medical Science)

基　　金：国家自然科学基金(30800466)

摘　　要：目的研究mAKAPβ蛋白在AngⅡ促新生大鼠心肌细胞肥大中的作用及其机制。方法观察AngⅡ刺激下大鼠心室肌细胞形态学变化及细胞内mAKAPβ蛋白表达水平的变化。使用RNA干扰技术抑制mAKAPβ蛋白表达,观察在此条件下AngⅡ促新生大鼠心肌细胞肥大作用的变化,同时观察ERK2蛋白磷酸化水平的变化。结果在AngⅡ刺激下,大鼠心肌细胞面积明显增大,ANP表达水平明显升高,P-ERK水平明显升高,但mAKAPβ蛋白表达水平无明显改变。使用RNA干扰技术抑制mAKAPβ蛋白表达后,AngⅡ促新生大鼠心肌细胞肥大的表现明显减弱甚至消失。结论 AngⅡ有明显的促新生大鼠心肌细胞肥大作用,mAKAPβ蛋白在此过程中发挥着重要作用。Objective To investigate the effect of mAKAPβ on AngⅡ-induced cardiac hypertrophy and its mechanism. Methods Cultured cardiomyocytes from neonatal rats were treated with AngⅡ,the morphology of cardiomyocytes were observed and the expression of mAKAPβwas measured. The mAKAPβ-shRNA was constructed for RNA interference, the expression of mAKAPβ in AngⅡ-treated rat cardiomyocytes was detected after RNA interference. The changes of ERK in cardiomyocytes were assessed before and after AngⅡ stimulation. Results In AngⅡ treated rat cardiac myocytes the areas of cells were larger than those of untreated cardiomyocytes, and the expression of hypertrophy marker ANP was higher in AngⅡ treated cells; however the expression level of mAKAPβ remained unchanged. RNA interference inhibited the expression of mAKAPβ protein, and the hypertrophy of cardiomyocyte induced by AngⅡwas attenuated. Conclusion AngⅡ can induce hypertrophy in rat cardiac myocytes, in which mAKAPβ protein is involved.

关 键 词：心肌细胞肥大 mAKAPβ蛋白 血管紧张素Ⅱ 大鼠 

分 类 号：R542.2[医药卫生—心血管疾病]