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Войти в исследования Allergy, asthma & immunology research · 2026
Cadherin-26 Promotes Airway Remodeling via Stabilizing Epithelial Expression of the Epidermal Growth Factor Receptor in Asthma.
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Gao Jiali, Chen Gongqi, Huang Chunli, Wang Zhen, Gu Wei, Jie Huiru, Xiong Tiantian, Feng Yuchen, Yi Lingling, Cheng Dan, Zhen Guohua
Аннотация
PURPOSE: Activation of epidermal growth factor receptor (EGFR) signaling in airway epithelial cells leads to epithelial-mesenchymal transformation (EMT) and airway remodeling in asthma. However, the mechanism regulating EGFR expression is not fully understood. We hypothesized that cadherin-26 (CDH26), a highly expressed cadherin in airway epithelium, promotes airway remodeling via regulating EGFR signaling in asthma.
METHODS: The expression of CDH26 in airway brush cells of asthmatic patients was examined using quantitative polymerase chain reaction. Airway hyperresponsiveness and remodeling were assessed in the house dust mite (HDM)-sensitized and -challenged Cdh26-deficient mice. The role and mechanism of CDH26 in epidermal growth factor (EGF)-induced EMT were measured in cultured human bronchial epithelial BEAS-2B cells.
RESULTS: The expression of CDH26 in airway brush cells was significantly correlated with the thickness of airway basement membrane in asthma patients. Cdh26 deficiency significantly reduced airway hyperresponsiveness and remodeling in HDM-sensitized and -challenged mouse model. In cultured human bronchial epithelial BEAS-2B cells, CDH26 knockdown inhibited EGF-induced EMT, whereas overexpression of CDH26 promoted EGF-induced EMT. Furthermore, CDH26 knockdown suppressed EGF-induced activation of EGFR signaling including phosphatidylinositol 3-kinase and AKT phosphorylation. By contrast, CDH26 overexpression intensified EGF-induced activation of EGFR signaling. Mechanistically, CDH26 knockdown promoted the proteasomal degradation of the EGFR.
CONCLUSIONS: CDH26 promoted airway remodeling via stabilizing the epithelial expression of EGFR and sustaining the activation of EGFR signaling in asthma. Thus, CDH26 can be a potential therapeutic target for airway remodeling in asthma.
METHODS: The expression of CDH26 in airway brush cells of asthmatic patients was examined using quantitative polymerase chain reaction. Airway hyperresponsiveness and remodeling were assessed in the house dust mite (HDM)-sensitized and -challenged Cdh26-deficient mice. The role and mechanism of CDH26 in epidermal growth factor (EGF)-induced EMT were measured in cultured human bronchial epithelial BEAS-2B cells.
RESULTS: The expression of CDH26 in airway brush cells was significantly correlated with the thickness of airway basement membrane in asthma patients. Cdh26 deficiency significantly reduced airway hyperresponsiveness and remodeling in HDM-sensitized and -challenged mouse model. In cultured human bronchial epithelial BEAS-2B cells, CDH26 knockdown inhibited EGF-induced EMT, whereas overexpression of CDH26 promoted EGF-induced EMT. Furthermore, CDH26 knockdown suppressed EGF-induced activation of EGFR signaling including phosphatidylinositol 3-kinase and AKT phosphorylation. By contrast, CDH26 overexpression intensified EGF-induced activation of EGFR signaling. Mechanistically, CDH26 knockdown promoted the proteasomal degradation of the EGFR.
CONCLUSIONS: CDH26 promoted airway remodeling via stabilizing the epithelial expression of EGFR and sustaining the activation of EGFR signaling in asthma. Thus, CDH26 can be a potential therapeutic target for airway remodeling in asthma.