Cardioprotective effect of estrogen and raloxifene
Project/Area Number |
14571560
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Obstetrics and gynecology
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Research Institution | Osaka University (2004) Yamagata University (2002-2003) |
Principal Investigator |
OHMICHI Masahide Osaka University, Graduate School of Medicine, Lecturer, 医学系研究科, 講師 (10283764)
|
Co-Investigator(Kenkyū-buntansha) |
TASAKA Keiichi Osaka University, Graduate School of Medicine, Associate professor, 医学系研究科, 助教授 (50155058)
TAHARA Masahiro Osaka University, Graduate School of Medicine, Assistant professor, 医学系研究科, 助手 (00294091)
TAKAHASHI Kazuhiro Yamagata University, Faculty of Medicine, Assistant professor, 医学部, 助手 (20292427)
SAKATA Masahiro Osaka University, Hospital, Associate professor, 医学部附属病院, 助教授 (10260639)
吉田 雅人 山形大学, 医学部, 助手 (20312738)
|
Project Period (FY) |
2002 – 2004
|
Project Status |
Completed (Fiscal Year 2004)
|
Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥900,000 (Direct Cost: ¥900,000)
|
Keywords | estrogen / raloxifene / vasodilatation / atherosclerosis / Akt / apoptosis / survival factor / ERα / 血管内皮機能 / 両側卵巣摘出術 / HUVEC / Survival factor / アポトーシス / 血管内皮細胞 / Akt |
Research Abstract |
Recent evidence suggests that the direct actions of estrogen on blood vessels contribute to the cardioprotective effects of estrogen. There are many kinds of direct effects of estrogen on blood vessels, such as estrogen-induced increases of vasodilatation and inhibition of the response of blood vessels to injury and the development of atherosclerosis. Although both estrogen and raloxifene activate NO synthesis in endothelial cells, the mechanism of inhibition of the response of blood vessels to injury by estrogen and raloxifene remains unclear. We identified that both estrogen and raloxifene decrease the apoptosis and act as a survival factor. Since blockage of Akt-BAD cascade by gene transfection and addition of inhibitor attenuated the decrement of apoptosis by estrogen and raloxifene, Akt-BAD cascade is involved in the inhibition of the response of blood vessels to injury by estrogen and raloxifene. Moreover, we identified that estrogen and raloxifene act as a survival factor thorough ERα, but not ERα Lastly, we examined the effect of surgical menopause on the function of vascular endothelium by brachial artery flow mediated dilatation. The function of vascular endothelium was significantly decreased after 1 week of surgical menopause.
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Report
(4 results)
Research Products
(7 results)