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COX-2-Derived Prostacyclin Confers Atheroprotection on Female Mice

McGuire Research Institute and The Department of Surgery, Virginia Commonwealth University, Ninth Floor, West Hospital, 1200 E. Broad St., Richmond, VA 23298-0108 simyers{at}vcu.edu

The authors report a study of the action of estrogen on estrogen receptor subtype cx to up-regulate the production of atheroprotective prostycyclin (PG61) by activation of cyclooxygenase-2 (COX-2). Oxidant stress and platelet activation that contribute to atherogenesis in female mice was restrained. The data suggest that the long-term use of selective COX-2 inhibitors could undermine protection from cardiovascular disease in women who are premenopausal.

Key Words: PGI • atherosclerosis • low-density-l poprotein receptor • cyclooxygenase-2

Perspectives in Vascular Surgery and Endovascular Therapy, Vol. 17, No. 3, 269-1-271 (2005)
DOI: 10.1177/153100350501700320


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