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Isoprostane-mediated secretion from human airway epithelial cells
1Department of Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia B3H 4H7, Canada. elizabeth.cowley@dal.ca
Molecular Pharmacology
|July 19, 2003
Summary
Isoprostanes, linked to reactive oxygen species, trigger anion secretion in airway epithelial cells. This finding suggests a role for isoprostanes in the lung
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Biochemistry
Background:
- Reactive oxygen species (ROS) cause lung tissue damage.
- Isoprostanes are products of polyunsaturated fatty acid peroxidation mediated by ROS.
- The role of isoprostanes in airway epithelial cell responses to oxidant stress is unclear.
Purpose of the Study:
- To investigate the effect of isoprostanes on human airway epithelial cells.
- To determine the mechanisms underlying isoprostane-induced responses in these cells.
- To explore the potential role of isoprostanes in pulmonary host defense.
Main Methods:
- Application of 8-iso-prostaglandin E2 (8-iso-PGE2) to Calu-3 cell monolayers.
- Measurement of transepithelial anion secretion via short circuit current (Isc).
- Electrophysiological studies on membrane preparations and receptor expression analysis (RT-PCR).
Main Results:
- 8-iso-PGE2 increased transepithelial anion secretion in Calu-3 cells.
- The response was greater with basolateral application and involved the cystic fibrosis transmembrane conductance regulator Cl- channel.
- 8-iso-PGE2 stimulated apical Cl- and basolateral K+ conductances, with both TP receptor-mediated and non-mediated effects observed.
Conclusions:
- This study is the first to show isoprostanes affecting airway epithelial cells.
- Isoprostanes modulate ion transport in airway epithelium.
- Isoprostanes may play a role in pulmonary host defense mechanisms.