期刊
RESPIROLOGY
卷 17, 期 7, 页码 1144-1149出版社
WILEY
DOI: 10.1111/j.1440-1843.2012.02228.x
关键词
air-liquid interface; airway epithelial cell; aquaporin; lipopolysaccharide; signalling pathway
资金
- National Science Foundation of China [B115, 81000012]
Background and objective: The aim of this study was to investigate the changes in expression of aquaporins (AQP) during differentiation of human bronchial epithelial cells and the role of lipopolysaccharide (LPS) in AQP expression. Methods: The levels of AQP3, AQP4 and AQP5 transcripts in human primary cultured bronchial epithelial cells were evaluated by real-time polymerase chain reaction at different time points before and after treatment with LPS. Western blotting was performed to assess the effects of LPS on AQP3, AQP4 and AQP5 expressions in normal human bronchial epithelial cells. Using pharmacological tools, the pathways involved in the regulation of LPS-induced changes in AQP5 were further explored. Results: The levels of AQP3, AQP4 and AQP5 transcripts were increased during differentiation of human bronchial epithelial cells. Expression of AQP5, but not AQP3 or AQP4, was downregulated by LPS. LPS-induced downregulation of AQP5 was inhibited by p38 and c-Jun N-terminal kinase (JNK) inhibitors. Conclusions: This study demonstrated that LPS decreases AQP5, but not AQP3 or AQP4, expression in human primary bronchial epithelial cells. The downregulation of AQP5 expression is mediated through a p38/JNK signalling pathway.
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