NDLI: A1 adenosine-receptor antagonists activate chloride efflux from cystic fibrosis cells.

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A1 adenosine-receptor antagonists activate chloride efflux from cystic fibrosis cells.

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A1 adenosine-receptor antagonists activate chloride efflux from cystic fibrosis cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Van Galen, P. J. Jacobson, K. A. Fox, C. Pollard, H. B. Cabantchik, Z. I. Turner, R. J. Eidelman, O. Guay-broder, C.
Description	Author Affiliation: Eidelman O ( Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892.);
Abstract	A1 adenosine-receptor-antagonist drugs such as 8-cyclopentyl-1,3-dipropylxanthine (CPX) and xanthine amine congener (XAC) are found to activate the efflux of 36Cl- from CFPAC cells. These cells are a pancreatic adenocarcinoma cell line derived from a cystic fibrosis (CF) patient homozygous for the common mutation, deletion of Phe-508. The active concentrations for these compounds are in the low nanomolar range, consistent with action on A1 adenosine receptors. In addition, drug action can be blocked by exogenous agonists such as 2-chloroadenosine and also can be antagonized by removal of endogenous agonists by treatment with adenosine deaminase. Cells lacking the CF genotype and phenotype, such as HT-29 and T84 colon carcinoma cell lines, appear to be resistant to activation of chloride efflux by either drug. CFPAC cells transfected with the CF transmembrane regulator gene, CFTR, are also resistant to activation by CPX. We conclude that, since these antagonists are of relatively low toxicity and appear to act somewhat selectively, they might be considered as promising therapeutic candidates for CF.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	12
Volume Number	89
Language	English
Publisher	National Academy of Sciences
Publisher Date	1992-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adenosine Analogs & Derivatives Pharmacology Chlorides Metabolism Cystic Fibrosis Physiopathology Purinergic Antagonists Xanthines 2-Chloroadenosine Adenocarcinoma Cell Line Chromosome Deletion Colonic Neoplasms Genetics Cystic Fibrosis Transmembrane Conductance Regulator Genotype Kinetics Membrane Proteins Mutation Pancreatic Neoplasms Phenotype Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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