European journal of medical research · 2025
Hypoxia disrupts human bronchial epithelial barrier integrity via tight junction protein remodeling and enhanced paracellular leakage.
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Huang Jianmin, He Shan, Zhang Qiuyun, Liu Yunliang, You Yongjing
Аннотация
BACKGROUND: Hypoxia can impair cell and organ function, and cause apoptosis and various diseases. At present, there are many studies on pulmonary hypoxia but few studies on bronchial injury. The study aimed to research the impact of hypoxia on the barrier function of human bronchial epithelial cells and the expression level of tight junction proteins.
METHODS: Primary human bronchial epithelial cells were allocated into four groups: (1) control group, (2) intermittent hypoxia group, (3) sustained hypoxia group, and (4) cigarette smoke exposure group. Apoptosis in each group was assessed by flow cytometric analysis. The expression levels of ZO-1, occludin, and claudin-1 were evaluated via Western blotting. Furthermore, trans-epithelial electrical resistance (TEER) was measured using an epithelial voltohmmeter to assess barrier function.
RESULTS: (1) Compared with the control group, the intermittent hypoxia group exhibited no significant differences in apoptosis rate, TEER, or the expression of tight junction proteins ZO-1, occludin, and claudin-1 (P > 0.05). In contrast, both the sustained hypoxia and cigarette smoke groups demonstrated significantly elevated apoptosis rates (P < 0.05). Claudin-1 expression was significantly reduced in the sustained hypoxia group (P < 0.05), while the increase in ZO-1 expression was not statistically significant (P > 0.05). In the cigarette smoke group, expression levels of ZO-1, occludin, and claudin-1 were all markedly decreased (P < 0.05). (2) Compared with the control group, TEER values were significantly reduced in both the sustained hypoxia and cigarette smoke groups (P < 0.05). (3) A significant difference in ZO-1 expression was observed between the sustained hypoxia and cigarette smoke groups (P < 0.05).
CONCLUSIONS: Hypoxia modulates the expression of tight junction proteins in human bronchial epithelial cells, disrupts intercellular junctional integrity, increases epithelial permeability, and ultimately impairs barrier function.
METHODS: Primary human bronchial epithelial cells were allocated into four groups: (1) control group, (2) intermittent hypoxia group, (3) sustained hypoxia group, and (4) cigarette smoke exposure group. Apoptosis in each group was assessed by flow cytometric analysis. The expression levels of ZO-1, occludin, and claudin-1 were evaluated via Western blotting. Furthermore, trans-epithelial electrical resistance (TEER) was measured using an epithelial voltohmmeter to assess barrier function.
RESULTS: (1) Compared with the control group, the intermittent hypoxia group exhibited no significant differences in apoptosis rate, TEER, or the expression of tight junction proteins ZO-1, occludin, and claudin-1 (P > 0.05). In contrast, both the sustained hypoxia and cigarette smoke groups demonstrated significantly elevated apoptosis rates (P < 0.05). Claudin-1 expression was significantly reduced in the sustained hypoxia group (P < 0.05), while the increase in ZO-1 expression was not statistically significant (P > 0.05). In the cigarette smoke group, expression levels of ZO-1, occludin, and claudin-1 were all markedly decreased (P < 0.05). (2) Compared with the control group, TEER values were significantly reduced in both the sustained hypoxia and cigarette smoke groups (P < 0.05). (3) A significant difference in ZO-1 expression was observed between the sustained hypoxia and cigarette smoke groups (P < 0.05).
CONCLUSIONS: Hypoxia modulates the expression of tight junction proteins in human bronchial epithelial cells, disrupts intercellular junctional integrity, increases epithelial permeability, and ultimately impairs barrier function.