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Papers In Press, published online ahead of print October 3, 2002
Cystic Fibrosis Research Laboratory, Stanford University, Stanford, CA 94305-2130
Corresponding Author: wine{at}stanford.edu
We are testing the hypothesis that malfunctioning of airway gland serous cells is a component of cystic fibrosis (CF) airway disease. CF is caused by mutations that disrupt CFTR, an anion channel essential for proper fluid secretion in some epithelia. Submucosal glands supply most of the mucus in upper airways, and gland serous cells are the primary site of CFTR expression in airways. We have discovered a major defect in CF glands by in situ optical monitoring of secretions from single human airway glands. CF glands did not secrete to agents that elevated [cAMP]
J. Biol. Chem, 10.1074/jbc.M208826200
Submitted on August 29, 2002
Revised on October 18, 2002
Accepted on October 3, 2002
Absent secretion to vasoactive intestinal peptide in cystic fibrosis airway glands
i, (0 responses /450 glands, 8 subjects) whereas glands were responsive in all donor tracheas (605/827 glands, 15 subjects) and in bronchi from subjects who were transplanted because of other lung diseases 148/166 glands, n =10). CF glands secreted to cholinergic stimulation, and serous cells were abundant in glands from all CF subjects. The complete absence of secretion to agents that elevate [cAMP]i suggests that altered secretion of gland mucus could contribute to CF lung disease.
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