| Project/Area Number |
18590937
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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 |
Neurology
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| Research Institution | Osaka University |
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Principal Investigator |
KITAGAWA Kazuo Osaka University, Graduate School of Medicine, Associate Professor (70301257)
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| Co-Investigator(Kenkyū-buntansha) |
HATAZAWA Jun Osaka University, Graduate School of Medicine, Professor (70198745)
YAGITA Yoshiki Osaka University, Graduate School of Medicine, Assistant Professor (20403066)
TOUDOU Kenichi Osaka University, Hospital, Resident (40403068)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,790,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥390,000)
Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2006: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | cerebral ischemia / collateral circulation / GM-CSF / chronic ischemia / arteriogenesis / 脳軟膜動脈吻合 / 顆粒球マクロファージコロニー刺激因子 / 脳梗塞 / 脳血流 / 慢性低灌流 / 脳血流自動調節 |
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| Research Abstract |
Granulocyte-macrophage colony stimulating factor (GM-CSF) has been reported to accelerate collateral growth (arteriogenesis) at the circle of Willis in rat brain. However, the effect of GM-CSF on leptomeninegal collateral growth has not been established. We examined the effect of unilateral common carotid artery (CCA) occlusion and GM-CSF treatment on leptomeninegal collateral growth in mice.
Adult mice were subjected to unilateral CCA occlusion or sham surgery followed by an alternate-day regimen of GM-CSF (20 μg/kg) or saline injection. On day 7, latex perfusion was performed in 1 set of mice to visualize the leptomeningeal vessels, and the number of Mac-2 (+) monocyte/macrophages on the dorsal surface of the brain was counted. In another set of mice, on day 7, permanent ipsilateral middle cerebral cerebral artery (MCA) occlusion was performed, and infarct volume was measured.
Leptomeningeal collateral growth was observed after CCA occlusion, and that was enhanced by GM-CSF treatment. An increase in the number of Mac-2(+) cells on the surface of the brain occurred after CCA occlusion and was enhanced by GM-CSF treatment. Seven days after CCA occlusion, GM-CSF treatment decreased the infarct size attributable to subsequent MCA occlusion.
After CCA occlusion, GM-CSF treatment enhanced leptomeningeal collateral growth and decreased the infarct size after MCA occlusion in mice.
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