Interaction between calcium-activated chloride channels and the cystic fibrosis transmembrane conductance regulator

We investigated interactions between cystic fibrosis conductance regulator (CFTR) and endogenous Ca2+-activated Cl- channels (CaCC) in bovine pulmonary artery endothelium (CPAE). CPAE cells, which do not express CFTR, were transiently transfected with wild-type (WT) CFTR and the deletion mutant delt...

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Bibliographic Details
Published in:Pflügers Archiv 1999-10, Vol.438 (5), p.635-641
Main Authors: Wei, L, Vankeerberghen, A, Cuppens, H, Eggermont, J, Cassiman, J J, Droogmans, G, Nilius, B
Format: Article
Language:English
Subjects:
1-Methyl-3-isobutylxanthine - pharmacology
Animals
Calcium - pharmacology
Cattle
Cell Line
Cell Membrane - physiology
Chloride Channels - physiology
Colforsin - pharmacology
Cystic Fibrosis Transmembrane Conductance Regulator - genetics
Cystic Fibrosis Transmembrane Conductance Regulator - physiology
Electric Conductivity
Endothelium, Vascular - metabolism
Gene Expression
Mutation
Pulmonary Artery - metabolism
Transfection
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Summary:We investigated interactions between cystic fibrosis conductance regulator (CFTR) and endogenous Ca2+-activated Cl- channels (CaCC) in bovine pulmonary artery endothelium (CPAE). CPAE cells, which do not express CFTR, were transiently transfected with wild-type (WT) CFTR and the deletion mutant deltaF508 CFTR. Currents through CaCC were significantly reduced after expression of WT CFTR. This inhibition was increased by stimulation (isobutylmethylxanthine, forskolin) of CFTR in cells expressing WT CFTR. There were no such effects when deltaF508 mutant CFTR, which is retained in the endoplasmic reticulum, was expressed. It is concluded that CFTR and CaCC are functionally coupled probably through a direct channel-channel interaction.
ISSN:0031-6768
1432-2013
DOI:10.1007/s004240051087