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

Erik M. Schwiebert, Marie E. Egan, Tae Ho Hwang, Stephanie B. Fulmer, Sandra S. Allen, Garry R. Cutting, William B. Guggino

Research output: Contribution to journalArticlepeer-review

Abstract

The cystic fibrosis transmembrane conductance regulator(CFTR) functions to regulate both CI- 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 [γ-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 C-.

Original languageEnglish (US)
Pages (from-to)1063-1073
Number of pages11
JournalCell
Volume81
Issue number7
DOIs
StatePublished - Jun 30 1995
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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