17&bgr;-estradiol inhibits proliferation of cultured vascular smooth muscle cells induced by lysophosphatidylcholine via a nongenomic antioxidant mechanism
作者:
Byung-Koo Yoon,
Won-Jong Oh,
Bruce Kessel,
Cheong-Rae Roh,
DooSeok Choi,
Je-Ho Lee,
Duk-Kyung Kim,
期刊:
Menopause
(OVID Available online 2001)
卷期:
Volume 8,
issue 1
页码: 58-64
ISSN:1072-3714
年代: 2001
出版商: OVID
关键词: Estrogen;Atherosclerosis;Antioxidant;Smooth muscle cell;Lysophosphatidylcholine
数据来源: OVID
摘要:
ObjectiveLysophosphatidylcholine (lysoPC), an active component of oxidized low-density lipoprotein, stimulates proliferation of vascular smooth muscle cells (VSMC). We investigated the direct impact of 17&bgr;-estradiol (E2) on the proliferation of VSMC from rat aorta.ResultsVSMC derived from both female and male rats expressed estrogen receptors &agr; and &bgr;. Treatments with 1% fetal bovine serum or 5 &mgr;M lysoPC increased the incorporation of [3H]-thymidine in VSMC obtained from female rats. 17&bgr;-E2did not alter the response to fetal bovine serum, but significantly suppressed the enhanced deoxyribonucleic acid synthesis which had been induced by lysoPC in a dose-dependent manner (10−14–10−6M). Estrogen also inhibited the proliferation of VSMC from male animals. ICI 182,780, a specific estrogen receptor antagonist, and 17&agr;-E2, an inactive form of estradiol, also decreased the mitogenic response to lysoPC in VSMC. In addition,N-acetyl-l-cysteine, a potent antioxidant, inhibited the lysoPC effect. Flow cytometric analysis using the oxidation-sensitive probe 2´,7´-dichlorofluorescin diacetate revealed that elevated intracellular formation of reactive oxygen species elicited with lysoPC was depressed significantly by 17&bgr;-E2, ICI 182,780, or 17&agr;-E2as well as byN-acetyl-l-cysteine.Conclusion17&bgr;-E2inhibits in vitro VSMC proliferation induced by lysoPC via a nongenomic antioxidant mechanism.
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