| Project/Area Number |
16K09523
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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 |
Cardiovascular medicine
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| Research Institution | Fukuoka University (2019)
Jikei University School of Medicine (2016-2018) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
宇都宮 一典 東京慈恵会医科大学, 医学部, 教授 (50185047)
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 動脈硬化 / 血管内皮機能 / Rho / mDia1 / Rho-kinase / 血管内皮 |
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| Outline of Final Research Achievements |
Atherosclerosis is known to occur due to vascular endothelial dysfunction. This study focused on mDia1 as a factor that regulates vascular endothelial function. mDia1 is an effector located downstream of small G protein Rho. Rho-kinase is known as an effector of Rho in addition to mDia1. We hypothesized that Rho-kinase and mDia1 interact with each other to regulate vascular endothelial function. We performed experimental studies using mice and cultured cells in which the endothelial ROCK2 isoform of Rho-kinase was deficient. It was revealed that mDia1 does not play a major role in the regulation of vascular endothelial function.
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| Academic Significance and Societal Importance of the Research Achievements |
低分子量GタンパクRhoに関連するシグナルとしては、動脈硬化の治療標的としてmDia1よりもROCK2がふさわしいことが明らかになった。今後はROCK2を標的とした創薬を行うことが動脈硬化治療における新たな戦略となり得る可能性が示された。
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