| Project/Area Number |
25461389
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Endocrinology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
AIHARA Ken-ichi 徳島大学, 大学院医歯薬学研究部, 特任教授 (70372711)
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Yasumasa 徳島大学, 大学院医歯薬学研究部, 准教授 (60432754)
YAGI Shusuke 徳島大学, 大学院医歯薬学研究部, 助教 (00507650)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | アンドロゲン受容体 / アンジオテンシンII / ApoE / 心筋肥大 / 動脈硬化 / マクロファージ / ノックアウトマウス / 性差 / 心血管病 |
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| Outline of Final Research Achievements |
Not only menopause but also andropause are critical issue to prevent the development of cardiovascular diseases in elderly people. In order to clarify the physiological role of androgen receptor (AR) in the process of cardiovascular remodeling, we studied mouse models of angiotensin II-infused female AR-deficient mice and macrophage-specific male AR-deficient mice. The values of cardiac hypertrophy and left ventricular interstitial fibrosis area showed no difference between the angiotensin II-infused female AR-deficient mice and wild type mice. In contrast, aortic adventitia hyperplasia was attenuated in AR-deficient female mice. In addition, macrophage specific AR-deficient male mice did not show the acceleration of atherosclerotic plaque area. Therefore, AR in macrophage was not associated with the development of atherosclerosis.
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