Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 98, Issue 24, Pages 14120-14125Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.241318498
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Funding
- NHLBI NIH HHS [HL60280-02, P50 HL060280] Funding Source: Medline
- NIDDK NIH HHS [KO1 DK02777-01] Funding Source: Medline
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Physical stimulation of airway surfaces evokes liquid secretion, but the events that mediate this vital protective function are not understood. When cystic fibrosis transmembrane conductance regulator (CFTR) channel activity was used as a functional readout, we found signaling elements compartmentalized at both extracellular and intracellular surfaces of the apical cell membrane that activate apical Cl- conductance in Calu-3 cells. At the outer surface, ATP was released by physical stimuli, locally converted to adenosine, and sensed by A(2B) adenosine receptors. These receptors couple to G proteins, adenylyl cyclase, and protein kinase A, at the intracellular face of the apical membrane to activate colocalized CFTR. Thus, airways have evolved highly efficient mechanisms to flush noxious stimuli from airway surfaces by selective activation of apical membrane signal transduction and effector systems.
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