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目的:通过研究新生大鼠体外培养的心肌细胞信号转导机制交叉对话,探讨心肌细胞肥大机制。方法:用血管紧张素Ⅱ(AngⅡ)和转化生长因子-β1(TGF-β1)及其相应的阻断剂Valsartan和Staurosporine刺激体外培养新生大鼠心肌细胞,以蛋白含量、搏动频率、细胞表面积等指标评价心肌细胞肥大。RT-PCR检测Smad3mRNA水平。Westernblotting检测磷酸化Stat1/Stat1,磷酸化Stat3/Stat3,Smad2/3。结果:AngⅡ(10-7mol/L)或者TGF-β1(3μg/L)刺激心肌细胞时,蛋白含量、搏动频率、细胞表面积呈现时间依赖方式的增加。与对照组相比,AngⅡ和TGF-β1刺激明显增加Smad3的mRNA水平。AngⅡ和TGF-β1刺激时,磷酸化Stat1/Stat1,磷酸化Stat3/Stat3,Smad2/3的增加可以被相应的阻断剂呈现时间依赖性逆转。结论:AngⅡ和TGF-β1通过Stat1,Stat3,和Samd2/3信号途径介导心肌细胞肥大。心肌细胞的信号转导交叉对话可以为心肌细胞肥大提供有效干预方法。
OBJECTIVE: To investigate the mechanism of cardiomyocyte hypertrophy by studying the cross-talk of cardiomyocyte signal transduction mechanism in neonatal rats. Methods: The neonatal rat cardiomyocytes were cultured in vitro with angiotensin Ⅱ (Ang Ⅱ) and transforming growth factor-β1 (TGF-β1) and its corresponding blockers Valsartan and Staurosporine. The protein content, pulsatile frequency, cell surface area Indexes to assess cardiomyocyte hypertrophy. The level of Smad3 mRNA was detected by RT-PCR. Western blotting detected phosphorylation of Stat1 / Stat1, phosphorylation of Stat3 / Stat3, Smad2 / 3. Results: The protein content, pulse frequency and cell surface area increased in a time-dependent manner when AngⅡ (10-7mol / L) or TGF-β1 (3μg / L) stimulated cardiomyocytes. Compared with the control group, AngⅡ and TGF-β1 stimulation significantly increased Smad3 mRNA levels. AngⅡ and TGF-β1 stimulation, phosphorylation of Stat1 / Stat1, phosphorylation Stat3 / Stat3, Smad2 / 3 increased by the corresponding blockers showed a time-dependent reversal. CONCLUSION: AngⅡ and TGF-β1 mediate cardiomyocyte hypertrophy through Stat1, Stat3, and Samd2 / 3 signaling pathways. Signal transduction of cardiomyocytes Cross-talk can provide an effective intervention for cardiomyocyte hypertrophy.