Effect of caveolin-1 on TGF-β1-induced epithelial-mesenchymal transition of human bronchial epithelial cells
10.3969/j.issn.1000-4718.2017.06.022
- VernacularTitle:Caveolin-1在TGF-β1诱导人支气管上皮细胞间质化中的作用
- Author:
Changjiang ZHONG
;
Jianhua LI
;
Xilei YUE
;
Jide XU
;
Chuntao YANG
;
Liting DENG
- Keywords:
Transforming growth factor β1;
Human bronchial epithelial cells;
Epithelial-mesenchymal transition;
Caveolin-1;
Airway remodeling
- From:
Chinese Journal of Pathophysiology
2017;33(6):1091-1097
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the role of caveolin-1 on epithelial-mesenchymal transition (EMT) in human bronchial epithelial (HBE) cells induced by transforming growth factor beta 1 (TGF-β1).METHODS:Immunofluorescence, real-time PCR and Western blot were applied to detect the mRNA and the protein expression of caveolin-1 in the 16HBE cells during EMT.The influence of siRNA-mediated silencing of caveolin-1 on EMT in the 16HBE cells was detected by Western blot.RESULTS:Caveolin-1 was widely present on the cell membrane of the 16HBE cells.The expression of caveolin-1 at mRNA and protein levels was significantly decreased in a time-dependent manner in the 16HBE cells compared with control group (P<0.05) after stimulation with TGF-β1.The morphologic changes of the 16HBE cells induced by TGF-β1 were promoted by caveolin-1 silencing compared with TGF-β1 group.The protein expression of E-cadherin and α-SMA induced by TGF-β1 was promoted by caveolin-1 silencing compared with TGF-β1 group (P<0.05).The phosphorylation levels of AKT and Smad3 were the highest at 30 min and increased significantly compared with control group (P<0.05) after stimulated with TGF-β1.Treatment of the 16HBE cells with TGF-β1 for 30 min after silencing caveolin-1 gene for 24 h significantly increased the phosphorylation levels of AKT and Smad3 compared with TGF-β1 group (P<0.05).CONCLUSION:TGF-β1 down-regulates the expression of caveolin-1 in the 16HBE cells.Caveolin-1 may participate in TGF-β1/Smad pathway and PI3K-AKT pathway, which are the signal transduction pathways for TGF-β1 inducing EMT.
