EP2receptor mediates bronchodilation by PGE2in mice

Autor: Sheller, J. R., Mitchell, Daphne, Meyrick, Barbara, Oates, John, Breyer, Richard
Zdroj: Journal of Applied Physiology; June 2000, Vol. 88 Issue: 6 p2214-2218, 5p
Abstrakt: PGE2is an important cyclooxygenase product that modulates airway inflammatory and smooth muscle responses. Signal transduction is mediated by four EP receptor subtypes that cause distinct effects on cell metabolism. To determine the role of EP2receptor activation, we produced a mouse lacking the EP2receptor by targeted gene disruption. The effect of aerosolized PGE2and other agonists was measured using barometric plethysmography and by measurements of lung resistance in mechanically ventilated mice. Inhalation of PGE2inhibited methacholine responses in wild-type but not in mice lacking the EP2receptor [EP2(−/−)]. After airway constriction was induced by methacholine aerosol, PGE2reduced the airway constriction enhanced pause in wild-type mice (from 0.88 ± 0.15 to 0.55 ± 0.06) but increased it in EP2(−/−) mice (from 0.73 ± 0.08 to 1.27 ± 0.19). Similar results were obtained in mechanically ventilated mice. These data indicate that the EP2receptor mediates the bronchodilation effect of PGE2.
Databáze: Supplemental Index