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A cyclic nucleotide PDE5 inhibitor corrects defective mucin secretion in submandibular cells containing antibody directed against the cystic fibrosis transmembrane conductance regulator protein
Author(s) -
McPherson Margaret A.,
Pereira Malcolm M.C.,
Lloyd Mills Chris,
Murray Kenneth J.,
Dormer Robert L.
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01672-5
Subject(s) - cystic fibrosis transmembrane conductance regulator , mucin , secretion , cystic fibrosis , cyclic nucleotide , chemistry , medicine , endocrinology , nucleotide , biology , biochemistry , gene
A selective cyclic nucleotide PDE5 inhibitor corrected the defective mucin secretion response to the β‐agonist isoproterenol in submandibular acinar cells inhibited by antibody directed against the cystic fibrosis transmembrane conductance regulator. The PDE5 inhibitor was as effective as cpt‐cyclic AMP or a selective PDE4 inhibitor. However, the PDE5 inhibitor had no effect on basal or isoproterenol‐stimulated cyclic AMP levels and did not stimulate mucin secretion. The results showing, for the first time, correction of the CFTR mucin secretion defect by a PDE5 inhibitor, which may involve cyclic GMP, will have a major impact in development of a rational drug treatment for cystic fibrosis.