| Project/Area Number |
23390234
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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 |
Neurology
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| Research Institution | Osaka University |
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Principal Investigator |
KITAGAWA KAZUO 大阪大学, 医学(系)研究科(研究院), 准教授 (70301257)
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| Co-Investigator(Kenkyū-buntansha) |
YAGITA Yoshiki 大阪大学, 医学系研究科, 助教 (20403066)
SASAKI Tsutomu 大阪大学, 医学部附属病院, 助教 (20534879)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥18,330,000 (Direct Cost: ¥14,100,000、Indirect Cost: ¥4,230,000)
Fiscal Year 2013: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2012: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥11,310,000 (Direct Cost: ¥8,700,000、Indirect Cost: ¥2,610,000)
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| Keywords | 側副血行 / 慢性脳低灌流 / 造血因子 / 高血圧 / 糖尿病 / 脳虚血 / インスリン抵抗性 / db/dbマウス / 慢性低潅流 / db/db マウス / 脳血流 |
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| Research Abstract |
Pial collateral development after chronic brain hypoperfusion, arteriogenesis, has attracted much attention because of potential therapeutic target in acute ischemic stroke. In this study, we have investigated the effect of granulocyte colony-stimulating factor (G-CSF), chronic hypertension and insulin resistance on pial collateral development in chronic brain hypoperfusion. In mice subjected to unilateral carotid occlusion, treatment with G-CSF enhanced pial collateral development and reduced infarct size after occlusion of middle cerebral artery. However, in both spontaneous hypertensive rats and db/db mice, no development of pial collateral circulation occurred after unilateral carotid occlusion. In conclusion, G-CSF could stimulate aretriogenesis in the pial circulation through recruitment of circulating monocytes, but arteriogenesis in chronic hypoperfusion would be hampered under the condition of endothelial dysfunction such as hypertension and insulin resistance.
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