| Project/Area Number |
25670125
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General pharmacology
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| Research Institution | Chiba University |
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Principal Investigator |
NISHIYAMA Mariko 千葉大学, 医学(系)研究科(研究院), 助教 (00092081)
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| Co-Investigator(Kenkyū-buntansha) |
KIMURA Sadao 千葉大学, 医学(系)研究科(研究院), 教授 (40134225)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | RGSタンパク質 / ウロテンシンII / アンジオテンシンII |
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| Outline of Final Research Achievements |
In the cardiovascular system, it is known that activation of urotensin II / urotensin II receptor signaling may serve as one of pathologically important mechanisms that may lead to cause or deteriorate various arteriosclerotic diseases. Factors that can suppress urotensin II receptor signaling may have anti-arteriosclerotic effects.
Urotensin II receptor is a G protein-coupled receptor (GPCR), and RGS proteins are intracellular negative regulators of GPCR signaling. In the present study, some particular R4/B family RGS proteins, such as RGS2, RGS3 and RGS8, were shown to have potent inhibitory effects on both urotensin II and angiotensin II signaling. Furthermore, important regions in these RGS molecules were specified. In particular, a C-terminal region of RGS8 was indicated to be crucial in the potent inhibitory activity. Agents that can increase intracellular amount of these RGS protein species are expected to become novel therapeutics in many types of arteriosclerotic diseases.
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