Abstract:
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, β-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.
journal_name
Respir Physiol Neurobioljournal_title
Respiratory physiology & neurobiologyauthors
Yu Z,Jiang Y,Sun Cdoi
10.1016/j.resp.2019.103283subject
Has Abstractpub_date
2020-01-01 00:00:00pages
103283eissn
1569-9048issn
1878-1519pii
S1569-9048(19)30149-1journal_volume
271pub_type
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