2023 Fiscal Year Final Research Report
Elucidation of the molecular basis of the small GTPase Rap1 governing the dynamic regulation of vascular permeability
| Project/Area Number |
21H02665
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 48020:Physiology-related
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| Research Institution | Nippon Medical School |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
寺井 健太 京都大学, 医学研究科, 准教授 (20616073)
高野 晴子 国立研究開発法人国立循環器病研究センター, 研究所, 上級研究員 (40532891)
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| Project Period (FY) |
2021-04-01 – 2024-03-31
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| Keywords | 血管透過性 / 血流 / 低分子量Gタンパク質Rap1 / 急性呼吸窮迫症候群 / 腫瘍血管 |
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| Outline of Final Research Achievements |
Endothelial cells lining the inner surface of blood vessels adhere to each other to form vascular barrier, thereby maintaining vascular permeability at a low level. However, during inflammation, vascular permeability temporarily increases as a part of defense mechanism. This study investigated the molecular mechanisms responsible for the dynamic regulation of vascular permeability and identified Rap1 small GTPase as a key intracellular signaling molecule to regulate vascular permeability. In particular, we demonstrate that Rap1 is essential for maintaining the barrier function of alveolar blood vessels. Additionally, we show that Rap1 has a protective role in conditions such as acute respiratory distress syndrome, where the barrier function of alveolar blood vessels is compromised.
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| Free Research Field |
血管生物学
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は、生体内における血管透過性の制御メカニズムを明らかにした点において、学術的に意義があります。また、急性呼吸窮迫症候群やがんなどの様々な疾患では、血管透過性が過剰に亢進することで病態が悪化することが知られています。本研究の成果は、これらの疾患において血管透過性が過剰に亢進する原因を理解するうえで重要な発見です。さらに、本研究の成果は、血管透過性の過剰亢進が関連する疾患の治療法開発に貢献することが期待されます。
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