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CFTR drives Na+-nHCO-3 cotransport in pancreatic duct cells: a basis for defective HCO-3 secretion in CF
Authors:Shumaker  Holli; Amlal  Hassane; Frizzell  Raymond; Ulrich  Charles D  II; Soleimani  Manoocher
Abstract:Pancreatic dysfunction in patients with cystic fibrosis (CF) isfelt to result primarily from impairment of ductalHCO-3 secretion. We provide molecularevidence for the expression of NBC-1, an electrogenicNa+-HCO-3cotransporter (NBC) in cultured human pancreatic ductcells exhibiting physiological features prototypical of CF ductfragments (CFPAC-1 cells) or normal duct fragments CAPAN-1 cellsand CFPAC-1 cells transfected with wild-type CF transmembraneconductance regulator (CFTR)]. We further demonstrate that1)HCO-3 uptake across the basolateralmembranes of pancreatic duct cells is mediated via NBC and2) cAMP potentiates NBC activitythrough activation of CFTR-mediatedCl- secretion. We proposethat the defect in agonist-stimulated ductal HCO-3 secretion in patients with CF ispredominantly due to decreased NBC-drivenHCO-3 entry at the basolateralmembrane, secondary to the lack of sufficient electrogenic drivingforce in the absence of functional CFTR.

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