COX-2-derived prostacyclin confers atheroprotection on female mice
KM Egan, JA Lawson, S Fries, B Koller, DJ Rader… - Science, 2004 - science.org
KM Egan, JA Lawson, S Fries, B Koller, DJ Rader, EM Smyth, GA FitzGerald
Science, 2004•science.orgFemale gender affords relative protection from cardiovascular disease until the menopause.
We report that estrogen acts on estrogen receptor subtype alpha to up-regulate the
production of atheroprotective prostacyclin, PGI2, by activation of cyclooxygenase 2 (COX-
2). This mechanism restrained both oxidant stress and platelet activation that contribute to
atherogenesis in female mice. Deletion of the PGI2 receptor removed the atheroprotective
effect of estrogen in ovariectomized female mice. This suggests that chronic treatment of …
We report that estrogen acts on estrogen receptor subtype alpha to up-regulate the
production of atheroprotective prostacyclin, PGI2, by activation of cyclooxygenase 2 (COX-
2). This mechanism restrained both oxidant stress and platelet activation that contribute to
atherogenesis in female mice. Deletion of the PGI2 receptor removed the atheroprotective
effect of estrogen in ovariectomized female mice. This suggests that chronic treatment of …
Female gender affords relative protection from cardiovascular disease until the menopause. We report that estrogen acts on estrogen receptor subtype alpha to up-regulate the production of atheroprotective prostacyclin, PGI2, by activation of cyclooxygenase 2 (COX-2). This mechanism restrained both oxidant stress and platelet activation that contribute to atherogenesis in female mice. Deletion of the PGI2 receptor removed the atheroprotective effect of estrogen in ovariectomized female mice. This suggests that chronic treatment of patients with selective inhibitors of COX-2 could undermine protection from cardiovascular disease in premenopausal females.
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