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Departments of 1 Biomedical Engineering, 2 Pediatrics, and 3 Medicine, Northwestern University, Evanston 60208; 4 Veterans Affairs Chicago Health Care System-Lakeside Division, Chicago, Illinois 60611; and 5 Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163
Repair of the airway epithelium after injury is critical for the maintenance of barrier function and the limitation of airway hyperreactivity. Airway epithelial cells (AECs) metabolize arachidonic acid to biologically active eicosanoids via the enzyme cyclooxygenase (COX). We investigated whether stimulating or inhibiting COX metabolites would affect wound closure in monolayers of cultured AECs. Inhibiting COX with indomethacin resulted in a dose-dependent inhibition of wound closure in human and feline AECs. Specific inhibitors for both COX-1 and COX-2 isoforms impaired wound healing. Inhibitors of 5-lipoxygenase did not affect wound closure in these cells. The addition of prostaglandin E2 (PGE2) eliminated the inhibition due to indomethacin treatment, and the exogenous application of PGE2 stimulated wound closure in a dose-dependent manner. Inhibition of COX with indomethacin only at initial time points resulted in a sustained inhibition of wound closure, indicating that prostanoids are involved in early wound repair processes such as spreading and migration. These differences in wound closure may be important if arachidonic acid metabolism and eicosanoid concentrations are altered in disease states such as asthma.
16HBE14o
cells; prostaglandin receptors; iloprost; enprostil; prostaglandin G/H synthase
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