2-methoxyestradiol, an endogenous metabolite of estrogen, enhances apoptosis and β-galactosidase expression in vascular endothelial cells

被引：71

作者：

Tsukamoto, A ^{[1
]}

Kaneko, Y ^{[1
]}

Yoshida, T ^{[1
]}

Han, K ^{[1
]}

Ichinose, M ^{[1
]}

Kimura, S ^{[1
]}

机构：

[1] Univ Tokyo, Fac Med, Dept Med 1, Bunkyo Ku, Tokyo 113, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1998年 / 248卷 / 01期

关键词：

D O I：

10.1006/bbrc.1998.8902

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

2-Methoxyestradiol (2ME) is an endogenous metabolite of estradiol (E2) and is known to inhibit tumor angiogenesis. In the present study, the direct effects of 2ME on the vascular endothelial cells were examined. 2ME enhanced apoptosis and beta-galactosidase expression in bovine vascular endothelial cells. A nitric oxide (NO) donor S-nitroso-N-acetyl penicillamin (SNAP) also enhanced beta-galactosidase expression, suggesting a possible role of NO in mediating the action of 2ME. 2ME increased the cellular content of nitric oxide synthase (NOS) and the production of NO. In addition, 2ME altered the membrane localization pattern of NOS. These suggest that the effects of 2ME on apoptosis and senescence of vascular endothelial cells were mediated, at least partly, by NOS and NO. (C) 1998 Academic Press.

引用

页码：9 / 12

页数：4

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