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Cell. 1995 Jun 30;81(7):1063-73.

CFTR regulates outwardly rectifying chloride channels through an autocrine mechanism involving ATP.

Author information

1
Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.

Abstract

The cystic fibrosis transmembrane conductance regulator (CFTR) functions to regulate both Cl- and Na+ conductive pathways; however, the cellular mechanisms whereby CFTR acts as a conductance regulator are unknown. CFTR and outwardly rectifying Cl- channels (ORCCs) are distinct channels but are linked functionally via an unknown regulatory mechanism. We present results from whole-cell and single-channel patch-clamp recordings, short-circuit current recordings, and [gamma-32P]ATP release assays of normal, CF, and wild-type or mutant CFTR-transfected CF airway cultured epithelial cells wherein CFTR regulates ORCCs by triggering the transport of the potent agonist, ATP, out of the cell. Once released, ATP stimulates ORCCs through a P2U purinergic receptor-dependent signaling mechanism. Our results suggest that CFTR functions to regulate other Cl- secretory pathways in addition to itself conducting Cl-.

PMID:
7541313
DOI:
10.1016/s0092-8674(05)80011-x
[Indexed for MEDLINE]
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