Activation effect of TGF-?_1 in human bronchial epithelial BEP2D cells on ERK MAPK pathway in signal transduction
- VernacularTitle:永生化人支气管上皮细胞中TGF-?_1对MAPK家族ERK通路的活化效应
- Author:
Qiao GOU
;
Boqiang SONG
;
Yingchun HU
- Publication Type:Journal Article
- Keywords:
human bronchial epithelial cells;
transforming growth factor beta;
mitogen-activated protein kinase kinases
- From:
Medical Journal of Chinese People's Liberation Army
2001;0(11):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of TGF-?1 on the activation of ERK MAPK in human bronchial epithelial BEP2D cells. Methods Western blot was employed to examine the time-dependent activation of ERK MAPK by TGF-?1. BEP2D cells were harvested after treatment of human bronchial epithelial cells with 2 ng/ml TGF-?1 for 0, 10, 30, 60, 120, 240 and 480 min, respectively. Fluorescent dye staining and flow cytometry were employed to assess the apoptosis of BEP2D cells treated with vehicle, or with 2ng/ml TGF-?1, or co-treated with 2ng/ml TGF-?1 and 5?M U0126. Proliferation of BEP2D cells treated with vehicle, or with 2ng/ml TGF-?1 or 5?M U0126, or co-treated with 2ng/ml TGF-?1 and 5?M U0126 was assayed with colony-forming test, respectively. Morphological observation was performed to observe the morphological changes in BEP2D cells treated with vehicle, or with 5ng/ml TGF-?1 or 5?M U0126, or co-treated with 5ng/ml TGF-?1 and 5?M U0126, respectively. Results TGF-?1 activated ERK MAPK in BEP2D cell. The maximal activation of ERK MAPK took place at 60min after stimulation with 2ng/ml TGF-?1. TGF-?1 treatment effectively inhibited cell proliferation, and induced their apoptosis and epithelial-mesenchymal transition. Pretreatment with U0126, an inhibitor of ERK MAPK, significantly enhanced the TGF-?1-mediated anti-proliferation and apoptosis effects, and inhibited the effect of epithelial-mesenchymal transition of TGF-?1 in BEP2D cells. Conclusion TGF-?1-induced phosphorylation of ERK MAPK may participate in BEP2D cell proliferation and apoptosis regulation.
