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学科主题: 临床医学
题名:
Estradiol improves cardiovascular function through up-regulation of SOD2 on vascular wall
作者: Liu, Zhaoyu1; Gou, Yulan2; Zhang, Hongyu3; Zuo, Houjuan1; Zhang, Haimou4; Liu, Zhengxiang1; Yao, Dachun1
关键词: Endothelium ; Estrogen receptor ; Gene therapy ; Mitochondrial function ; Reactive oxygen species
刊名: REDOX BIOLOGY
发表日期: 2014
DOI: 10.1016/j.redox.2014.11.001
卷: 3, 页:88-99
收录类别: SCI
文章类型: Article
关键词[WOS]: ESTROGEN-RECEPTOR-ALPHA ; ENDOTHELIAL DYSFUNCTION ; FEMALE MICE ; MITOCHONDRIAL DYSFUNCTION ; OXIDATIVE STRESS ; HORMONE-THERAPY ; DEFICIENT MICE ; OBESITY ; DISEASE ; BETA
英文摘要:

Epidemiological studies have shown that estrogens have protective effects in cardiovascular diseases, even though the results from human clinical trials remain controversial, while most of the animal experiments confirmed this effect, but the detailed mechanism remains unclear. In this study, we found that estradiol (E2) treatment significantly increases the expression of mitochondrial superoxide dismutase (SOD2) in mice and in vitro in human aorta endothelial cells. Further investigation shows that E2 up-regulates SOD2 through tethering of estrogen receptor (ER) to Sp1 and the increased binding of Sp1 to GC-box on the SOD2 promoter, where ER alpha responses E2-mediated gene activation, and ER beta maintains basal gene expression level. The E2/ER-mediated SOD2 up-regulation results in minimized ROS generation, which highly favors healthy cardiovascular function. Gene therapy through lentivirus-carried endothelium-specific delivery to the vascular wall in high-fat diet (HET) mice shows that the SOD2 expression in endothelial cells normalizes E2 deficiency-induced ROS generation with ameliorated mitochondrial dysfunction and vascular damage, while SOD2 knockdown worsens the problem despite the presence of E2, indicating that E2-induced SOD2 expression plays an important vasculoprotective role. To our knowledge, this is the first report for the mechanism by which E2 improves cardiovascular function through up-regulation of SOD2 in endothelial cells. In turn, this suggests a novel gene therapy through lentivirus-carried gene delivery to vascular wall for E2 deficiency-induced cardiovascular damage in postmenopausal women. (C) 2014 The Authors. Published by Elsevier B.V.

语种: 英语
所属项目编号: 2013 DEA31400
项目资助者: International Science &amp ; Technology Cooperation Project of Ministry of Education, China
WOS记录号: WOS:000350812500012
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/52315
Appears in Collections:北京大学深圳医院_血液内科_期刊论文

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作者单位: 1.Wuhan 1 Hosp, Dept Neurol, Wuhan 430022, Peoples R China
2.Hubei Univ, Sch Life Sci, Wuhan 430062, Peoples R China
3.Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Internal Med, Wuhan 430030, Peoples R China
4.Peking Univ, ShenZhen Hosp, Dept Hematol, Shenzhen 518036, Peoples R China

Recommended Citation:
Liu, Zhaoyu,Gou, Yulan,Zhang, Hongyu,et al. Estradiol improves cardiovascular function through up-regulation of SOD2 on vascular wall[J]. REDOX BIOLOGY,2014,3:88-99.
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