| Project/Area Number |
10670643
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | NAGOYA UNIVERSITY |
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Principal Investigator |
HIRAKI Makoto SCHOOL OF MEDICINE, ASSISTANT PROFESSOR, 医学部, 講師 (90242875)
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| Co-Investigator(Kenkyū-buntansha) |
KADOMATSU Kenji SCHOOL OF MEDICINE, Associate Professor, 医学部, 助教授 (80204519)
MURAMATSU Takashi SCHOOL OF MEDICINE, PROFESSOR, 医学部, 教授 (00030891)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1998: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | atherosclerosis / chemotaxis / growth substances / inflammation / knockout mice / ミッドカイン(MK) / 新生内膜増殖 / PTN |
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| Research Abstract |
Neointimal formation is a common feature of atherosclerosis and restenosis after balloon angioplasty. To find a new target to suppress neointima formation, we investigated the possible role of midkine (MK), a heparin-binding growth factor with neurotrophic and chemotactic activities, in neointima formation. MK expression increased during neointima formation caused by intraluminal balloon injury of the rat carotid artery. Neointima formation in a restenosis model was strongly suppressed in MK-deficient mice. Continuous administration of MK protein to MK-deficient mic restored neointima formation. Leukocyte recruitment to the vascular walls after injury was markedly decreased in MK-deficient mice. Soluble MK as well as that bound to the substratum induced migration of macrophages in vitro. These results indicate that MK plays a critical role in neointima formation at least in part due to its ability to mediate leukocyte recruitment.
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