Glucocorticoids inhibits the repair of airway epithelial cells via the activation of wnt pathway

被引:6
|
作者
Yu, Zhongcui [1 ]
Jiang, Yubo [1 ]
Sun, Congling [1 ]
机构
[1] Yantai Hosp Tradit Chinese Med, Dept Pediat, 39 Xingfu Rd, Yantai, Shandong, Peoples R China
关键词
Wnt pathway; Asthma; Glucocorticoids; Airway epithelial cells; BETA-CATENIN; ASTHMA; MODEL; EXPRESSION; PROMOTES;
D O I
10.1016/j.resp.2019.103283
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Background: The purpose of this study was to explore the effect of Wnt pathway on the inhibition of airway epithelial cells repair by glucocorticoid. Materials and Methods: The expression of E-cadherin in asthma mice model was detected by immunocytochemistry. XAV939 was used to treat 16HBE, and the expressions of related genes were determined by western blotting and quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, migration and cell cycle were analyzed by methylthiazolyldiphenyl-tetrazolium bromide, wound healing and flow cytometry, respectively. Results: In asthma mice model, the lung tissue was impaired. After dexamethasone treatment, the airway inflammation was relieved and the expression of E-cadherin was reduced. Dexamethasone increased the expressions of Wnt7b, LRP5, beta-catenin and CyclinD1, inhibited cell viability and migration and arrested cell cycle, whereas XAV939 produced the opposite effects. In addition, XAV939 suppressed Wnt pathway that activated by dexamethasone. Conclusion: Glucocorticoid could inhibit cell proliferation and migration via regulating Wnt pathway to affect cell cycle, thus inhibiting the repair of airway epithelial after injury.
引用
收藏
页数:8
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