Caveolin-1在TGF-β1诱导人支气管上皮细胞间质化中的作用

发布时间：2018-05-29 15:04

本文选题：转化生长因子β + 人支气管上皮细胞　；参考：《中国病理生理杂志》2017年06期

【摘要】：目的:探究小窝蛋白1(caveolin-1)在转化生长因子β1(TGF-β1)诱导的人支气管上皮细胞(16HBE细胞)上皮-间充质转化(EMT)中的作用。方法:以16HBE细胞株为研究对象,免疫荧光、RT-q PCR和Western blot实验检测16HBE细胞EMT过程中caveolin-1的mRNA和蛋白表达;Western blot检测siRNA干扰caveolin-1对16HBE细胞EMT的影响。结果:Caveolin-1广泛存在于16HBE细胞膜上,TGF-β1刺激后,caveolin-1的mRNA和蛋白表达减少(P0.05)。与TGF-β1组比较,caveolin-1 siRNA和TGF-β1共同作用促进了细胞形态的转化,抑制了E-钙黏蛋白的蛋白表达而促进了α-SMA的蛋白表达(P0.05)。TGF-β1刺激16HBE细胞后,AKT和Smad3在30 min磷酸化水平最高,与0 min对照组比较显著增加(P0.05);用siRNA干扰caveolin-1基因后再用TGF-β1刺激16HBE细胞30 min,下游信号蛋白分子AKT和Smad3的磷酸化水平增高,与TGF-β1组比较显著增加(P0.05)。结论:TGF-β1能下调16HBE细胞的caveolin-1表达水平;caveolin-1可能参与了TGF-β1诱导的16HBE细胞EMT过程中TGF-β1/Smad通路和PI3K-AKT通路的活化。
[Abstract]:Aim: to investigate the role of fossa protein 1 caveolin-1 in epithelial-mesenchymal transformation (EMTT) induced by transforming growth factor 尾 1 (TGF- 尾 1) in human bronchial epithelial cells (TGF- 尾 1). Methods: the expression of mRNA and protein of caveolin-1 in EMT of 16HBE cells was detected by immunofluorescence RT-q PCR and Western blot assay. The effect of siRNA interference caveolin-1 on EMT of 16HBE cells was detected by Western blot. Results the expression of mRNA and protein of TGF- 尾 1 in 16HBE cells was decreased after the stimulation of TGF- 尾 1. Compared with TGF- 尾 1 group, the co-action of TGF- 尾 1 siRNA and TGF- 尾 1 promoted the transformation of cell morphology, inhibited the protein expression of Ecadherin, and promoted the expression of 伪 -SMA protein. The phosphorylation levels of AK T and Smad3 in 16HBE cells stimulated by TGF- 尾 1 and TGF- 尾 1 were the highest at 30 min. Compared with 0 min control group, the level of phosphorylation of AKT and Smad3 increased significantly in 16HBE cells after siRNA interference with caveolin-1 gene and then stimulated with TGF- 尾 1 for 30 min, and the phosphorylation level of AKT and Smad3 increased significantly compared with TGF- 尾 1 group, and the phosphorylation level of TGF- 尾 1 increased significantly as compared with that of TGF- 尾 1 group. Conclusion: TGF- 尾 1 can down-regulate the expression of caveolin-1 in 16HBE cells. Caveolin-1 may be involved in the activation of TGF- 尾 1/Smad pathway and PI3K-AKT pathway in 16HBE cells induced by TGF- 尾 1.
【作者单位】：广州市花都区人民医院;广州医科大学生理学教研室;黄石市中心医院;
【基金】：国家自然科学基金资助项目(No.81470205)
【分类号】：R562.25

【相似文献】