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膜雌激素受体 alpha（ERα）以配体非依赖的方式参与血流介导的扩张。

Membrane estrogen receptor alpha (ERα) participates in flow-mediated dilation in a ligand-independent manner.

机构信息

Angers University, MITOVASC, CNRS UMR 6015, INSERM U1083, Angers, France.

CARFI facility, Angers University, Angers, France.

出版信息

Elife. 2021 Nov 29;10:e68695. doi: 10.7554/eLife.68695.

DOI:10.7554/eLife.68695
PMID:34842136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8676342/
Abstract

Estrogen receptor alpha (ERα) activation by estrogens prevents atheroma through its nuclear action, whereas plasma membrane-located ERα accelerates endothelial healing. The genetic deficiency of ERα was associated with a reduction in flow-mediated dilation (FMD) in one man. Here, we evaluated ex vivo the role of ERα on FMD of resistance arteries. FMD, but not agonist (acetylcholine, insulin)-mediated dilation, was reduced in male and female mice lacking ERα (-/- mice) compared to wild-type mice and was not dependent on the presence of estrogens. In C451A-ERα mice lacking membrane ERα, not in mice lacking AF2-dependent nuclear ERα actions, FMD was reduced, and restored by antioxidant treatments. Compared to wild-type mice, isolated perfused kidneys of C451A-ERα mice revealed a decreased flow-mediated nitrate production and an increased HO production. Thus, endothelial membrane ERα promotes NO bioavailability through inhibition of oxidative stress and thereby participates in FMD in a ligand-independent manner.

摘要

雌激素受体 α（ERα）通过其核作用激活雌激素，从而防止动脉粥样硬化，而位于质膜的 ERα 则加速内皮愈合。一个人的 ERα 基因缺失与血流介导的扩张（FMD）减少有关。在这里，我们评估了 ERα 在阻力血管 FMD 中的作用。与野生型小鼠相比，缺乏 ERα（-/- 小鼠）的雄性和雌性小鼠的 FMD 降低，而激动剂（乙酰胆碱、胰岛素）介导的扩张不受雌激素的影响。在缺乏膜 ERα 的 C451A-ERα 小鼠中，而不是在缺乏 AF2 依赖性核 ERα 作用的小鼠中，FMD 降低，并且抗氧化剂治疗可使其恢复。与野生型小鼠相比，C451A-ERα 小鼠的分离灌注肾脏显示出降低的血流介导的硝酸盐产生和增加的 HO 产生。因此，内皮膜 ERα 通过抑制氧化应激来促进 NO 的生物利用度，从而以配体非依赖性方式参与 FMD。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94f0/8676342/24d0a6cfff3e/elife-68695-fig9.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94f0/8676342/24d0a6cfff3e/elife-68695-fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94f0/8676342/01ab670e64d9/elife-68695-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94f0/8676342/3986938457c1/elife-68695-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94f0/8676342/59e06ad50372/elife-68695-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94f0/8676342/09204bc27e3a/elife-68695-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94f0/8676342/26a226807963/elife-68695-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94f0/8676342/d19800ea5da5/elife-68695-fig4-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94f0/8676342/c9575f962fbc/elife-68695-fig5.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94f0/8676342/8c207f2b81a6/elife-68695-fig7-figsupp1.jpg
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