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

Objective: 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.

Conclusions: 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.