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目的:研究生长因子胰岛素样生长因子-Ⅰ(IGF-Ⅰ)、巨噬一粒细胞集落刺激因子(GM-CSF)和表皮生长因子(EGF)对核心结合因子α1(Cbfα1)的调节作用及其与有丝分裂原激活蛋白激酶(MAPK)信号转导通路的关系。方法:采用报告基因方法和RT-PCR技术检测Cbfα1基因启动子活性及mRNA表达的变化。结果:在MC3T3-E1细胞中,IGF-Ⅰ(1 nmol/L 1μmol/L)、GM-CSF(100 nmol/L)和EGF(1μmol/L)作用24小时能够增加Cbfα1基因启动子活性(P<0.05),加入PD98059(10μmol/L)后不但抑制了Cbfα1基因启动子活性的基础表达,而且完全阻断了IGF-1、GM-CSF和EGF所诱导的Cbfα1基因启动子活性的增加(P<0.01),在C2C12细胞中得到了类似结果,另外,MC3T3-E1和C2C12细胞分别经IGF-Ⅰ(1,100 nmol/L)、GM-CSF (100 nmol/L,1μmol/L)和EGF(1 μmol/L,100 nmol/L)处理后均使Cbfα1基因mRNA表达水平提高(P<0.05),而加入PD98059 可抑制上述因子的刺激作用。结论:IGF-Ⅰ、GM-CSF和EGF能够刺激MC3T3E1和C2C12细胞中小鼠Cbfα1基因启动子活性及mRNA的表达,此作用可能经MAPK信号传导通路介导。
AIM: To investigate the regulatory effect of IGF-Ⅰ, GM-CSF and EGF on the expression of Cbfα1 And mitogen-activated protein kinase (MAPK) signal transduction pathway. Methods: The promoter activity and mRNA expression of Cbfα1 gene were detected by reporter gene method and RT-PCR. Results: The effect of IGF-Ⅰ (1 μmol / L 1 μmol / L), GM-CSF (100 nmol / L) and EGF (1 μmol / L) for 24 h on the promoter activity of Cbfα1 gene in MC3T3- <0.05), PD98059 (10μmol / L) not only inhibited the basic expression of Cbfα1 promoter activity but also completely blocked the increase of promoter activity of Cbfα1 gene induced by IGF-1, GM-CSF and EGF Similar results were obtained in C2C12 cells. In addition, MC3T3-E1 and C2C12 cells were treated with IGF-I (1,100 nmol / L), GM-CSF (100 nmol / L, μmol / L, 100 nmol / L) could increase the mRNA expression of Cbfα1 (P <0.05), while PD98059 could inhibit the above stimulation. CONCLUSION: IGF-Ⅰ, GM-CSF and EGF can stimulate the promoter activity and mRNA expression of Cbfα1 in MC3T3E1 and C2C12 cells, which may be mediated by MAPK signal transduction pathway.