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    Science. 2004 Dec 10;306(5703):1954-7. Epub 2004 Nov 18.

    COX-2-derived prostacyclin confers atheroprotection on female mice.

    Egan KM, Lawson JA, Fries S, Koller B, Rader DJ, Smyth EM, Fitzgerald GA.

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    Institute for Translational Medicine and Therapeutics, University of Pennsylvania, PA 19104, USA.

    Abstract

    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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    PMID:
    15550624
    [PubMed - indexed for MEDLINE]

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