中文摘要：

为了探讨在人永生化支气管上皮细胞BEP2D细胞中,Smad4分子对ERK/MAPK通路的作用,我们用RNA干扰的方法分别设计了两对Smad4-siRNA,并使BEP2D细胞中Smad4靶向沉默,用Western印迹分析了细胞内ERK激酶和MEK激酶磷酸化水平的变化.结果发现,当Smad4表达沉默后,ERK激酶磷酸化水平未变,MEK激酶磷酸化水平有所降低;再加TGF-β1诱导后ERK激酶和MEK激酶磷酸化水平均显著降低至基础水平以下.结果表明在BEP2D细胞中,Smad4的缺失抑制TGF-β1对ERK/MAPK通路的活化,故提出TGF-β活化ERK/MAPK通路需要Smad4存在的假设.

英文摘要：

To investigate the function of Smad4 in ERK/MAPK signaling pathway in human bronchial epithelial BEP2D cells, siRNAs were designed to specifically target Smad4 in BEP2D cells, siRNA transfection and western blots were performed to examine the phosphorylation levels of ERK and MEK. The results showed that Smad4 gene silencing leads to the phosphorylation level of MEK1 but not ERK decreased. After stimulation with TGF-β1, phosphorylation levels of both ERK and MEK are decreased and lower than the control cells. The results demonstrated that Smad4 is participating in the activation of the ERK/MAPK signaling by TGF-β1.