Role of cAMP-PKA/CREB pathway in regulation of AQP 5 production in rat nasal epithelium

Abstract

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. 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. 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. 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.