| Autor: |
Cathapermal S; Department of Physiology and Biophysics, Georgetown University Medical Center, Washington, DC 20007, USA., Lavigne MC, Leong-Son M, Alibadi T, Ramwell PW |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of cardiovascular pharmacology [J Cardiovasc Pharmacol] 1998 Apr; Vol. 31 (4), pp. 499-505. |
| DOI: |
10.1097/00005344-199804000-00005 |
| Abstrakt: |
An in vitro xanthine/xanthine oxidase reaction system was used to generate superoxide anions that significantly stimulated tritiated [3H]thymidine incorporation into endothelium-removed (denuded) male rat aortic explants. Tritiated thymidine uptake was used as an index of vascular smooth-muscle cell (VSMC) proliferation. Superoxide dismutase (SOD) significantly attenuated the oxygen free radical-induced proliferative response of these cells. 17Beta-estradiol (17beta-E) significantly inhibited superoxide anion-induced VSMC proliferation. In contrast, the growth-modifying effects of 17beta-E were not mimicked by 17alpha-estradiol (17alpha-E), progesterone, or testosterone. The pure estrogen receptor (ER) antagonist, ICI 164,384, reversed the growth-inhibitory effect of 17beta-E. 17Beta-estradiol failed directly to reduce in vitro superoxide anion production or to modify xanthine oxidase activity. Therefore, these data indicate that 17beta-E, through an ER-dependent mechanism, specifically and significantly inhibited superoxide anion-mediated SMC proliferation in denuded rat aortic explants. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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