The prostaglandin E₂ type 4 receptor participates in the response to acute oxidant stress in airway epithelial cells

The Journal of Pharmacology and Experimental Therapeutics
Christina L JonesElizabeth A Cowley

Abstract

Oxidative stress is implicated in the pathogenesis of many inflammatory pulmonary diseases, including cystic fibrosis (CF). Delineating how oxidative stress stimulates CF transmembrane conductance regulator (CFTR) in airway epithelial cells is useful, both to increase the understanding of airways host defense and suggest therapeutic approaches to reduce the oxidant stress burden in the CF lung. Using the airway epithelial cell line Calu-3, we investigated the hypothesis that hydrogen peroxide (H₂O₂), which stimulates anion efflux through CFTR, does so via the production of prostaglandin E₂ (PGE₂). Using iodide efflux as a biochemical marker of CFTR activity and short circuit current (I(sc)) recordings, we found that the H₂O₂-stimulated efflux was abolished by cyclooxygenase-1 inhibition and potentially also involves microsomal prostaglandin E synthase-1 activity, implicating a role for PGE₂ production. Furthermore, H₂O₂ application resulted in a rapid release of PGE₂ from Calu-3 cells. We additionally hypothesized that the PGE₂ subtype 4 (EP(4)) receptor was involved in mediating this response. In the presence of (4Z)-7-[(rel-1S,2S,5R)-5-((1,1'-biphenyl-4-yl)methoxy)-2-(4-morpholinyl)-3-oxocyclopentyl]-4-heptenoic acid (AH23848...Continue Reading

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Jun 8, 2013·American Journal of Respiratory Cell and Molecular Biology·Gregory E ConnerMatthias Salathe
Jun 8, 2013·Prostaglandins & Other Lipid Mediators·Bogdan JakielaMarek Sanak
Oct 12, 2018·American Journal of Physiology. Cell Physiology·Scott M O'Grady
Oct 6, 2017·American Journal of Physiology. Cell Physiology·Francis H WongJohn W Hanrahan

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