Role of store-operated Ca2+ entry in house dust mites-induced dysfunction of airway epithelial barrier in asthmatic mice
Objective:To investigate the potential role and mechanisms of store-operated Ca2+ entry(SOCE)-mediated calcium signaling in airway epithelial barrier dysfunction of asthmatic mice.Methods:C57BL/6 mice were divided into the control group,asthma model group,and asthma mod-el group treated with SOCE blocker BTP-2.Acute allergic asthma models were established with house dust mite(HDM)sensitization and challenge.Lung inflammation was evaluated by HE stain-ing.Enzyme-linked immunosorbent assay(ELISA)was used to assess the levels of IL-13 in bron-choalveolar lavage fluid(BALF)and IgE in serum.The airway epithelial integrity was evaluated by the FITC-dextran permeability test.The expression of ZO-1 and occludin in airway epithelial was evaluated with immunofluorescence and histochemistry,and the mRNA and protein expression of ZO-1 and occludin in lung tissue was evaluated by RT-PCR and Western Blot.Results:The airway in-flammation in asthmatic mice was aggravated as compared with the mice in control group.Compared with the control mice,the mRNA and protein levels of ZO-1 and occludin in lung tissue were signifi-cantly reduced,and the permeability of FTIC-dextran was increased in asthmatic mice(P＜0.000 1).BTP-2 treatment significantly reduced the airway inflammation,increased the mRNA and protein ex-pression of ZO-1 and occludin,and decreased the permeability of FTIC-dextran in asthmatic mice(P＜0.000 1).Conclusion:SOCE may participate in HDM-induced dysfunction of the airway epithelial barrier in asthmatic mice.
House Dust MiteAirway Epithelial BarrierStore-Operated Calcium EntryAsthmaAirway Inflammation
NETL
NSTL
万方数据
维普
