| Project/Area Number |
25460906
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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 |
General internal medicine(including psychosomatic medicine)
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| Research Institution | Yokohama City University |
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Principal Investigator |
KANAOKA Tomohiko 横浜市立大学, 医学(系)研究科(研究院), 客員研究員 (70551258)
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| Co-Investigator(Kenkyū-buntansha) |
TOYA Yoshiyuki 横浜市立大学, 附属病院, 准教授 (30237143)
TAMURA Kouichi 横浜市立大学, 医学部, 准教授 (40285143)
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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 |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 受容体 / シグナル伝達 / 生理活性 / 循環器・高血圧 / トランスレーショナルリサーチ / 生体分子 |
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| Outline of Final Research Achievements |
In the course of an investigational search for a fine means to regulate AT1R signaling at the local tissue sites, we have focused our analysis on the AT1R-associated protein (ATRAP), which is a molecule that directly binds to the carboxyl‐terminal domain of AT1R. In contrast to the classical components of the renin-angiotensin system (i.e. angiotensinogen, renin and AT1R), alteration of ATRAP expression exerts no evident effects on baseline BP and renal morphology and function in vivo such as in ATRAP-transgenic mice and ATRAP-deficient mice in physiological condition. However, accumulating experimental results in these mice indicate that ATRAP exerts inhibitory effects on the exaggerated activation of tissue AT1R signaling in response to pathological stimuli, in order to protect cardiovascular and renal tissues under pathological conditions, in spite of no influence of ATRAP on physiological AT1R signaling.
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