| Project/Area Number |
18K08360
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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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| Review Section |
Basic Section 54010:Hematology and medical oncology-related
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| Research Institution | Ehime University |
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Principal Investigator |
Hato Takaaki 愛媛大学, 医学系研究科, 研究員 (30172943)
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| Co-Investigator(Kenkyū-buntansha) |
山之内 純 愛媛大学, 医学部附属病院, 准教授 (10423451)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 血小板 / G蛋白質 / 血栓性素因 / 血小板減少 |
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| Outline of Final Research Achievements |
We found a large family with congenital thrombocytopenia and arteriovenous thrombosis and identified mutation of a G protein-coupled receptor, GPR25. Patients had enhanced platelet aggregation and blood coagulation on the platelet surface. Mice bearing this mutation did not have constant abnormal findings. However, patient’s platelets showed enhanced thrombopoiesis, suggesting early platelet destruction. This study suggests that GPR25 activates platelets and promotes platelet thrombus formation, and that such activated platelets are removed early from the systemic circulation.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究はGPR25が血小板活性化に関連した新たな血小板膜蛋白受容体であることを示唆している。GPR25の知見は血小板減少症および血栓症の新たな治療薬の開発戦略の基盤になると思われる。さらに、GPR25は受容体蛋白質の構造を有しているが、その生理的リガンドは知られていない。このリガンドは血小板活性化に関連していると思われるので、GPR25へのリガンド結合阻害薬は有力な抗血栓薬となる可能性がある。それ故、本研究の成果は将来の創薬につながる可能性がある。
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