Local regulation of cystic fibrosis transmembrane regulator and epithelial sodium channel in airway epithelium.

Pingbo Huang, Elaine Gilmore, Patricia Kultgen, Paul Barnes, Sharon Milgram, M. Jackson Stutts

Research output: Contribution to journalReview articlepeer-review

33 Scopus citations

Abstract

Regulation of cystic fibrosis transmembrane regulator (CFTR) and epithelial sodium channel (ENaC) in airway epithelia strongly influences the rate of mucociliary clearance (MCC) by determining the volume of airway surface liquid. MCC increases in response to stimuli originating on the airway surface, and CFTR and ENaC in airway epithelia appear to be regulated by local rather than systemic signaling. Although all signals that regulate CFTR and ENaC in airways have not been identified, the release of nucleotides from airway epithelial cells exposed to physical stimuli initiates a series of events that coordinately favor increased MCC. These events include activation of adenosine A2B receptors that stimulate CFTR and P2Y2 receptors that inhibit ENaC. Together these actions result in an increased volume of airway surface liquid and increased MCC rates. Stimulation of CFTR by A(2B)AR uses protein kinase (PK) A signaling elements that are localized within the apical/subapical compartment, including G proteins, adenylyl cyclase, PKA-II, A-kinase anchoring proteins, and phosphodiesterases. Inhibition of ENaC by P2Y2 receptors appears to be mediated by phospholipase C-beta3, possibly through an effect on the levels of phosphatidylinositol 4,5-bisphosphonate in the apical membrane.

Original languageEnglish (US)
Pages (from-to)33-37
Number of pages5
JournalProceedings of the American Thoracic Society
Volume1
Issue number1
DOIs
StatePublished - 2004
Externally publishedYes

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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