| Project/Area Number |
21590244
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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 |
General physiology
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| Research Institution | Nagahama Institute of Bio-Science and Technology (2010-2011)
Kinki University (2009) |
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Principal Investigator |
NAGAI Nobuo 長浜バイオ大学, バイオサイエンス学部, 教授 (90260281)
|
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| Co-Investigator(Kenkyū-buntansha) |
KAWAO Naoyuki 近畿大学, 医学部, 助教 (70388510)
OKADA Kiyotaka 近畿大学, 医学部, 講師 (20185432)
MATSUO Osamu 近畿大学, 医学部, 名誉教授 (40030879)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 病態生理 / uPAR / 脳梗塞 / 血管透過性 / 血管新生 / ウロキナーゼレセプター / ウロキナーゼ / 血管内皮細胞 / 脳定量障害モデル / bEnd.3 / 酸素グルコース除去 / 酸素グルコース除 |
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| Research Abstract |
In the present study we observed that mice with gene deficient of uPAR had lower blood-brain barrier(BBB) permeability increase after ischemic stroke than their wild type control, suggesting that uPAR deteriorates ischemic brain damage via increase in BBB permeability. In addition, as mechanisms, we found that the increase in the BBB permeability just after ischemic damage was associated with the increase in the permeability of preexisting vessels but the increase in the permeability observed inside of damage at 1 week was associated with newly generated vessels which did not interact with astrocytes.
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