COX-2-Derived Prostacyclin Confers Atheroprotection on Female Mice
| Autor: | John A. Lawson, Susanne Fries, Garret A. FitzGerald, Daniel J. Rader, Emer M. Smyth, Karine Egan, Beverly H. Koller |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
Male
medicine.medical_specialty Arteriosclerosis medicine.drug_class Ovariectomy Myocytes Smooth Muscle Alpha (ethology) Estrogen receptor Prostacyclin Biology Receptors Epoprostenol Antioxidants Muscle Smooth Vascular Lactones Mice Internal medicine medicine Animals Cyclooxygenase Inhibitors Sulfones Platelet activation Receptor Cells Cultured Mice Knockout Sex Characteristics Multidisciplinary Cyclooxygenase 2 Inhibitors Estradiol Estrogen Receptor alpha Hydrogen Peroxide Platelet Activation medicine.disease Epoprostenol Isoenzymes Mice Inbred C57BL Menopause Oxidative Stress Endocrinology Receptors LDL Cardiovascular Diseases Cyclooxygenase 2 Prostaglandin-Endoperoxide Synthases Estrogen biology.protein Female Lipid Peroxidation Cyclooxygenase medicine.drug |
| Zdroj: | Science. 306:1954-1957 |
| ISSN: | 1095-9203 0036-8075 |
| DOI: | 10.1126/science.1103333 |
| Popis: | 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, PGI 2 , 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 PGI 2 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
| Nepřihlášeným uživatelům se plný text nezobrazuje | K zobrazení výsledku je třeba se přihlásit. |