Effects of Wnt/β-catenin signal pathway on asthma airway remodeling
10.3969/j.issn.1000-4718.2017.09.024
- VernacularTitle:Wnt/β-catenin信号通路调控哮喘气道重塑的机制研究
- Author:
xiao Xiao JIA
1
;
ying Rong ZHENG
;
Yue HUANG
;
yu Ze ZENG
;
xi Wei ZHANG
Author Information
1. 温州医科大学附属第二医院
- Keywords:
Asthma;
Airway remodeling;
Airway smooth muscle cells;
Wnt/β-catenin signaling pathway;
β-catenin
- From:
Chinese Journal of Pathophysiology
2017;33(9):1683-1689
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To explore the effect of Wnt/β-catenin signaling pathway in airway smooth muscle cells (ASMC) on asthmatic airway remodeling.METHODS:The asthmatic airway remodeling model in rats was established and the ASMC was isolated and cultured.The protein expression of β-catenin,glycogen synthase kinase-3β (GSK-3β),cMyc and cyclin D1 in the ASMC was determined by Western blot.After depressing the interaction between β-catenin and p300/CBP,the cell activity was measured by CCK-8 assay and the change of cell cycle distribution was analyzed by flow cytometry.Meanwhile,the protein expression of c-Myc and cyclin D1 in the ASMC was determined by Western blot after inhibiting P38 mitogen-activated protein kinase (MAPK) activity.RESULTS:The protein levels of β-catenin,c-Myc and cyclin D1 were significantly increased in asthma group while the protein level of GSK-3β was decreased in the same group (P ＜ 0.05).After depressing the interaction between β-catenin and p300/CBP,the cell activity of ASMC was decreased in asthma group compared with control group (P ＜ 0.05),and the change of the cell cycle distribution in asthma group was also more obvious (P ＜ 0.05).After inhibiting P38 MAPK activity,the protein levels of c-Myc and cyclin D1 were all decreased compared with control group in ASMC asthma and control rats (P ＜ 0.05).CONCLUSION:Wnt/β-catenin signaling pathway may participates in airway remodeling in asthma by increasing the protein expression of c-Myc and cyclin D1,reacting with the P38 MAPK signaling pathway and regulating the growth of ASMC.
