Open AccessRole of cAMP-PKA/CREB pathway in regulation of AQP 5 production in rat nasal epithelium
Author(s) -
W Wang,
Miaoyan Zheng
Publication year - 2011
Publication title -
rhinology (amsterdam. online)/rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.275
H-Index - 57
eISSN - 1996-8604
pISSN - 0300-0729
DOI - 10.4193/rhino10.107
Subject(s) - creb , forskolin , cyclic adenosine monophosphate , protein kinase a , adenosine , blot , microbiology and biotechnology , medicine , biology , endocrinology , kinase , biochemistry , transcription factor , receptor , gene
OBJECTIVES: Aquaporin 5 (AQP5) is a water-specific channel protein. In this study, we investigated the possible role of the cyclic adenosine monophosphate-protein kinase A/cyclic adenosine monophosphate response element binding protein (cAMP-PKA/CREB) pathway in the regulation of AQP5 in nasal epithelial cells. METHODS: Rat nasal epithelial cells were cultured and treated with the PKA inhibitor H89 or cAMP inducing medicine forskolin for 12 or 24 hours in vitro. AQP5 and phosphorylated CREB (p-CREB) at serine133 (Ser133) were detected by immunocytochemistry, Western blotting or real-time PCR. Experiments were repeated 10 times. RESULTS: After treatment with H89 for 12 or 24 hours, the number of cells positive for AQP5 and p-CREB (Ser133) were decreased, p-CREB (Ser133) and AQP5 protein decreased, and AQP5 mRNA decreased. After treatment with forskolin for 12 or 24 hours, the number of p-CREB (Ser133) and AQP5 positive cells increased, p-CREB (Ser133) and AQP5 protein increased, and AQP5 mRNA was increased. CONCLUSION: Both H89 (PKA inhibitor) and forskolin (cAMP inducing medicine) regulate AQP5 production through the cAMP-PKA/CREB pathway, which could influence the secretory function of the submucosal glands in nasal epithelium.