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secretion via CFTR
in Calu-3 airway epithelial cells
Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03755
Cystic fibrosis is
caused by mutations in the cystic fibrosis transmembrane conductance
regulator (CFTR) Cl
channel, which mediates transepithelial
Cl transport in a variety
of epithelia, including airway, intestine, pancreas, and sweat duct. In
some but not all epithelial cells, cAMP stimulates
Cl secretion in part by
increasing the number of CFTR
Cl channels in the apical
plasma membrane. Because the mechanism whereby cAMP stimulates CFTR
Cl secretion is cell-type
specific, our goal was to determine whether cAMP elevates CFTR-mediated
Cl secretion across serous
airway epithelial cells by stimulating the insertion of CFTR
Cl channels from an
intracellular pool into the apical plasma membrane. To this end we
studied Calu-3 cells, a human airway cell line with a serous cell
phenotype. Serous cells in human airways, such as Calu-3 cells, express
high levels of CFTR, secrete antibiotic-rich fluid, and play a critical
role in airway function. Moreover, dysregulation of CFTR-mediated
Cl secretion in serous
cells is thought to contribute to the pathophysiology of cystic
fibrosis lung disease. We report that cAMP activation of CFTR-mediated
Cl secretion across human
serous cells involves stimulation of CFTR channels present in the
apical plasma membrane and does not involve the recruitment of CFTR
from an intracellular pool to the apical plasma membrane.
cystic fibrosis; serous cell; submucosal gland; chloride transport; cystic fibrosis transmembrane conductance regulator
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