| Project/Area Number |
20390268
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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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| Research Field |
Hematology
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| Research Institution | University of Yamanashi |
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Principal Investigator |
OZAKI Yukio University of Yamanashi, 大学院・医学工学総合研究部, 教授 (30134539)
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Katsue 山梨大学, 大学院・医学工学総合研究部, 准教授 (10324211)
INOUE Osamu 山梨大学, 大学院・医学工学総合研究部, 助教 (00432154)
SATOH Kaneo 山梨大学, 医学部, 助手 (20242662)
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| Co-Investigator(Renkei-kenkyūsha) |
ASADA Yujiro 宮崎大学, 医学部, 教授 (70202588)
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| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥9,490,000 (Direct Cost: ¥7,300,000、Indirect Cost: ¥2,190,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2008: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
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| Keywords | 血小板 / CLEC-2 / ポドプラニン / 血栓症 / podoplanin / 動脈硬化 / 動脈血栓症 |
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| Research Abstract |
Novel platelet activation receptor CLEC-2 binds to podoplanin expressed on the surface of several kinds of cancer cells, which facilitates cancer metastasis. However, its role in thrombosis and hemostasis has not been elucidated to date. We generated CLEC-2-deficient mice and found that thrombus formation was inhibited in vivo and in vitro. We also found that CLEC-2 forms homophilic association in a manner depending on platelet activation, which stabilizes thrombus formation. Tail bleeding was not significantly increased in CLEC-2-deficient platelets, suggesting that CLEC-2 may be a good target protein for anti-platelet drug, which inhibits pathological thrombosis, but not physiological hemostasis.
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