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学科主题: 基础医学
题名:
Estrogen-receptor-mediated protection of cerebral endothelial cell viability and mitochondrial function after ischemic insult in vitro
作者: Guo, Jiabin1,2,3; Krause, Diana N.1; Horne, James1; Weiss, John H.4; Li, Xuejun2,3; Duckles, Sue P.1
关键词: estrogen protection ; estradiol ; cerebral ischemia and/or reperfusion
刊名: JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
发表日期: 2010-03-01
DOI: 10.1038/jcbfm.2009.226
卷: 30, 期:3, 页:545-554
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Endocrinology & Metabolism ; Hematology ; Neurosciences
研究领域[WOS]: Endocrinology & Metabolism ; Hematology ; Neurosciences & Neurology
关键词[WOS]: BLOOD-BRAIN-BARRIER ; PRECONDITIONING PROTECTS ; OXIDATIVE STRESS ; WORKING GROUP ; BETA ; STROKE ; INJURY ; ALPHA ; NEUROPROTECTION ; ESTRADIOL
英文摘要:

Protective effects of estrogen against experimental stroke and neuronal ischemic insult are well-documented, but it is not known whether estrogen prevents ischemic injury to brain endothelium, a key component of the neurovascular unit. Increasing evidence indicates that estrogen exerts protective effects through mitochondrial mechanisms. We previously found 17 beta-estradiol (E2) to improve mitochondrial efficiency and reduce mitochondrial superoxide in brain blood vessels and endothelial cells. Thus we hypothesized E2 will preserve mitochondrial function and protect brain endothelial cells against ischemic damage. To test this, an in vitro ischemic model, oxygen-glucose deprivation (OGD)/reperfusion, was applied to immortalized mouse brain endothelial cells (bEnd.3). OGD/reperfusion-induced cell death was prevented by long-term (24, 48 h), but not short-term (0.5, 12 h), pretreatment with 10 nmol/L E2. Protective effects of E2 on endothelial cell viability were mimicked by an estrogen-receptor (ER) agonist selective for ER alpha (PPT), but not by one selective for ER beta (DPN). In addition, E2 significantly decreased mitochondrial superoxide and preserved mitochondrial membrane potential and ATP levels in early stages of OGD/reperfusion. All of the E2 effects were blocked by the ER antagonist, ICI-182,780. These findings indicate that E2 can preserve endothelial mitochondrial function and provide protection against ischemic injury through ER-mediated mechanisms. Journal of Cerebral Blood Flow & Metabolism (2010) 30, 545-554; doi: 10.1038/jcbfm.2009.226; published online 28 October 2009

语种: 英语
所属项目编号: R01 HL-50775 ; 20073020 ; 2004CB518902
项目资助者: United States National Heart, Lung and Blood Institute ; Chinese Government Scholarships for Postgraduates ; 973 Program of the Ministry of Science and Technology in China
WOS记录号: WOS:000275108900010
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/63335
Appears in Collections:基础医学院_药理学系_期刊论文

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作者单位: 1.Univ Calif Irvine, Dept Pharmacol, Sch Med, Irvine, CA 92697 USA
2.Peking Univ, Sch Basic Med Sci, Dept Pharmacol, Beijing 100871, Peoples R China
3.Peking Univ, State Key Lab Nat Biomimet Drugs, Beijing 100871, Peoples R China
4.Univ Calif Irvine, Dept Neurol, Sch Med, Irvine, CA 92697 USA

Recommended Citation:
Guo, Jiabin,Krause, Diana N.,Horne, James,et al. Estrogen-receptor-mediated protection of cerebral endothelial cell viability and mitochondrial function after ischemic insult in vitro[J]. JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM,2010,30(3):545-554.
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