NEW YORK (Reuters Health) - Prostacyclin, a prostaglandin formed, in part, by cyclooxygenase-2 (COX-2), protects against atherogenesis in female mice, new research shows. Moreover, estrogen increases the formation of COX-2-derived prostacyclin.
If these findings hold true in humans, selective COX-2 inhibitors, such as rofecoxib and celecoxib, may “undermine protection from cardiovascular disease in premenopausal females,” senior author Dr. Garret A. FitzGerald, from the University of Pennsylvania in Philadelphia, and colleagues note.
Although premenopausal women are known to be at decreased risk for cardiovascular disease, the mechanisms involved are unclear, according to the report in the November 18th online issue of Sciencexpress.
In the new study, Dr. FitzGerald’s team shows that by acting on estrogen receptor-alpha, estrogen activates COX-2, which, in turn, increases the production of prostacyclin.
Further analysis showed that the anti-atherosis effect worked against both oxidant stress and platelet activation, the researchers note. Moreover, the benefits of prostacyclin were lost in animals lacking the prostacyclin receptor.
The current findings could have important implications for juvenile arthritis, a disease that typically affects females and can be treated with COX-2 inhibitors. In addition, the findings may have “implications for the design and interpretation of trials of hormone replacement therapy,” the authors state.
Source: Sciencexpress 2004. [ Google search on this article ]
MeSH Headings:Animal Diseases: Disease Models, Animal: DiseasesCopyright © 2002 Reuters Limited. All rights reserved. Republication or redistribution of Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Reuters. Reuters shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon. Reuters and the Reuters sphere logo are registered trademarks and trademarks of the Reuters group of companies around the world.
