Estrogen modulation of endothelium-derived relaxing factors by human endothelial cells
Estrogen modulation of endothelium-derived relaxing factors by human endothelial cells
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DOI：
10.1016/j.bbrc.2004.07.137
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发表时间：
2004-09-17
影响因子：
3.1
通讯作者：
van Breemen, C
中科院分区：
文献类型：
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作者：
Rahimian, R;Chan, L;van Breemen, C
我们报告了雌激素对人内皮细胞系EA.hy926释放内皮源性舒张因子（EDRFs）的调节作用。使用生物测定，我们表明EA.hy926释放EDRF，包括一氧化氮（NO）和内皮源性超极化因子（EDHF），通过松弛预收缩的去内皮兔主动脉环来测量。17-β-雌二醇（10（-6）mol/L）处理24 h后，细胞内EDRF的生成量明显高于对照组。此外，L-NAME的细胞灌流液引起的内皮细胞灌流液诱导的松弛，成为短暂的，并取消由于雌激素治疗的松弛增强。在灌流液中加入K-Ca通道阻滞剂可阻断L-NAME对生物测定环的抑制作用。使用实时荧光PCR，我们证明，eNOS的表达在雌激素处理的细胞显着高于对照组。这些结果表明，雌激素通过刺激NO而不是EDHF的产生来发挥潜在的重要血管保护作用。(C)2004年爱思唯尔公司All rights reserved.
We report the modulatory effects of estrogen on release of endothelium-derived relaxing factors (EDRFs) in a human endothelial cell line, EA.hy926. Using bioassay, we showed that EA.hy926 released EDRF including nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) measured by relaxation of pre-contracted endothelium-denuded rabbit aortic rings. This EDRF production was significantly higher in cells treated for 24 h with 17-beta-estradiol (10(-6) mol/L) than control cells. Addition of L-NAME to the perfusate of cells caused the relaxation induced by the endothelial cell perfusate to become transient and abolished the enhancement of relaxation due to estrogen treatment. Addition of K-Ca channel blockers to the perfusate abolished the L-NAME-resistant relaxation of the bioassay ring. Using real-time PCR, we demonstrated that eNOS expression in estrogen-treated cells was significantly higher than controls. These results show that estrogen exerts a potentially important vasculo-protective effect by stimulating NO but not EDHF production. (C) 2004 Elsevier Inc. All rights reserved.