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目的:探讨TGF-β_1诱导的大鼠心肌细胞肥大中钙调素依赖蛋白激酶Ⅱ信号途径的信号表达。方法:建立TGF-β_1诱导的体外大鼠心肌细胞肥大模型PI染色标记细胞双链RNA法检测心肌细胞RNA表达量,间接检测心肌细胞肥大。实时荧光定量PCR检测心肌细胞肥大相关基因肌球蛋白重链β亚型(β-MHC)的表达。Western blotting检测心肌细胞中p-CaMKⅡ蛋白表达。结果:TGF-β_1可诱导体外培养心肌细胞肥大基因的表达,β-MHC的表达明显高于对照组(P<0.01)。PI染色TGF-β_1组PI含量明显增高(P<0.01),TGF-β_1 3μg/L组心肌细胞内PI含量最高(80.57±3.56);与对照组相比,TGF-β_1可明显上调的表达p-CaMKⅡ(108.83±12.15 vs 10.6±1.35,P<0.01),并于TGF-β_1诱导2 h表达达峰。结论:TGF-β_1可诱导心肌细胞肥大的形成,此过程中CaMKⅡ蛋白表达明显增加。
AIM: To investigate the signal transduction pathway of calmodulin-dependent protein kinase Ⅱ (TGF-β1) -induced cardiomyocyte hypertrophy in rats. Methods: The expression of RNA in cardiomyocytes was detected by double stranded RNA polymerase chain reaction (PI) staining of cardiomyocyte hypertrophy model induced by TGF-β 1 in vitro. Cardiomyocyte hypertrophy was detected indirectly. Real-time fluorescence quantitative PCR was used to detect the expression of myosin heavy chain β-subunit (β-MHC) in cardiomyocyte hypertrophy related genes. Western blotting was used to detect the expression of p-CaMKII protein in cardiomyocytes. Results: TGF-β 1 induced cardiomyocyte hypertrophy gene expression in vitro, the expression of β-MHC was significantly higher than that of the control group (P <0.01). The content of PI in PI-stained TGF-β1 group was significantly higher than that in control group (P <0.01), and the highest level of PI was found in TGF-β 1 3μg / L group (80.57 ± 3.56) -MaKKⅡ (108.83 ± 12.15 vs 10.6 ± 1.35, P <0.01), and peaked at 2 h after TGF-β 1 induction. CONCLUSION: TGF-β 1 can induce cardiomyocyte hypertrophy, and the expression of CaMKⅡ protein is significantly increased in this process.