TGF-β1及其信号蛋白Smad3对大鼠心肌细胞肥大的作用

目的：探讨转化生长因子β1（transforming growth factor,TGF-β1）及其信号蛋白Smad3在诱导大鼠心肌细胞肥大中的作用。 方法： 培养新生大鼠心肌细胞，流式细胞仪检测心肌细胞总蛋白含量，RT-PCR法检测胚胎抗原ANF mRNA（atrial natriuretic factor）及Smad3 mRNA的表达，Western blotting检测Smad3蛋白的表达。 结果： 不同浓度TGF-β1均能明显增加心肌细胞总蛋白含量和ANF mRNA的表达, Smad3基因反义寡核苷酸能抑制TGF-β1诱导的心肌细胞肥大，TGF-β1诱导肥大的心肌细胞内信号蛋白Smad3表达的增加。 结论： TGF-β1及其信号蛋白Smad3可能参与诱导大鼠心肌细胞肥大的病理过程。

Effects of TGF-β1 and signal protein Smad3 on rat cardiac myocyte hypertrophy

AIM: To investigate the effects of TGF-β1 and signal protein Smad3 on rat cardiac myocyte hypertrophy. METHODS: The total protein was analyzed by flow cytometry and the ANF mRNA expression was measured by RT-PCR to judge the hypertrophy of cultured neonatal cardiac myocytes. Smad3 mRNA expression in cardiac myocytes was measured by RT-PCR, and the protein expression of Smad3 was analyzed by Western blotting. RESULTS: TGF-β1 significantly increased the total protein in cardiac myocytes and promoted ANF mRNA expression, compared with control group. In cultured neonatal myocytes, AS-ODN of Smad3 inhibited myocyte hypertrophy induced by TGF-β1. Smad3 mRNA and protein expression increased at 15 min after incubated with TGF-β1, reached the peak at 1 h, and declined at 4 h. CONCLUSION: TGF-β1 and signal protein Smad3 may participate in the progress of rat cardiac myocyte hypertrophy.