Dataset of KCNQ1, KCNN4, KATP channel expression and dexamethasone modulation of protein kinase signaling in airway epithelial cells

Dexamethasone produces anti-secretory responses in airway epithelium through the inhibition of basolateral membrane K+ channels [1–3]. We have used the human bronchial epithelial cell line 16HBE14o− to investigate the effects of dexamethasone on the expression of K+ channels and regulatory protein kinases. The data demonstrate the expression of three distinct K+ channel types – KCNQ1:KCNE3, KCNN4 and KATP which are differentially regulated by protein kinase A and protein kinase C. The data also provide evidence for rapid non-genomic actions of dexamethasone on PKC and PKA phosphorylation and their association with the various K+ channel sub-types. Biotinylation experiments provide data on the effects of dexamethasone on membrane expression of the K+ channels. Antibody co-immunoprecipitation, rtPCR and western blotting data are given for the non-genomic dexamethasone transcription-cell signaling pathway involving Gi-protein coupled receptor, PKC, adenylyl cyclase Type IV, cAMP, PKA and ERK1/2 activation. Keywords: Dexamethasone, Non-genomic, Airway epithelium, KCNQ1, KCNN4, KATP channels, Protein kinases