CFTR-independent prostaglandin E 2 -stimulated chloride secretion in human airway

uses EP4 prostanoid receptor-mediated activation of Src, phosphoinositol phosphate (PI3K), and serum glucocorticoid kinase 1 (SGK1) to stimulate cystic fibrosis transmembrane conductance regulator (CFTR)-independent, calcium-activated chloride secretion through apical calcium release-activated calcium channels, P2X receptors, and basolateral TRPV channels in Calu-3 submucosal gland airway cells. These findings provide new potential targets to bypass airway chloride secretory defects in lung diseases with compromised CFTR function.