| Project/Area Number |
20790671
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Hematology
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| Research Institution | University of Yamanashi |
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Principal Investigator |
INOUE Osamu University of Yamanashi, 医学部附属病院, 助教 (00432154)
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| Research Collaborator |
SUZUKI-INOUE Katsue 山梨大学, 大学院・医学工学総合研究部, 准教授 (10324211)
OZAKI Yukio 山梨大学, 大学院・医学工学総合研究部, 教授 (30134539)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 血栓 / 止血学 / CLEC-2 / 医学 / 血栓止血 / 血小板 / CARD9 |
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| Research Abstract |
C-type lectin like receptor 2 (CLEC-2) is a novel platelet activating receptor. We are trying to elucidate the physiological role and signaling mechanism of CLEC-2. CARD-9 is an adaptor protein that plays a role in signalling downstream of another C-type lectin like receptor dectin-1. The platelet aggregation induced by a CLEC-2 specific agonist rhodocytin was not altered in the absence of CARD-9, suggesting that CARD-9 is not involved in the signaling mechanism downstream of CLEC-2. Although we have successfully generated CLEC-2 deficient mice, they were almost embryonic lethal. Since some of CLEC-2 null fetus can survive around E15, we further performed transplantation of liver cells of CLEC-2 null fetus to recipient mice that were irradiated to kill the hematopoietic stem cells in the bone marrow, and made chimera mice that have CLEC-2 deficient blood cells including platelets. Our CLEC-2 chimera mice successfully produce CLEC-2 deficient blood and we can investigate the physiological role of CLEC-2 using these mice. We are going to isolate bone marrow megakaryocytes from the chimera mice next and try to identify the role of CLEC-2 in megakaryopoiesis and platelet production.
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