| Project/Area Number |
16590855
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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 | Hyogo College of Medicine |
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Principal Investigator |
NISHIMURA Hiroyuki Hyogo College of Medicine, Faculty of Medicine, Assistant Professor, 医学部, 講師 (20248131)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUYAMA Tomohiro Hyogo College of Medicine, Faculty of Medicine, Professor, 医学部, 教授 (10219529)
YOSHIKAWA Hiroo Hyogo College of Medicine, Faculty of Medicine, Professor, 医学部, 教授 (90273680)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | cerebral ischemia / angiogenesis / neurogenes / progenitor cell / neuronal function / CD34 / 血管内皮前駆 |
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| Research Abstract |
Thrombo-occlusive cerebrovascular disease resulting in stroke and permanent neuronal loss is an important cause of morbidity and mortality. Because of the unique properties of cerebral vasculature and the limited reparative capability of neuronal tissue, it has been difficult to devise effective neuroprotective therapies in cerebral ischemia. We developed the cerebral ischemic model. The model is highly reproducible and survives for more than twelve weeks. Using this model, we demonstrated that systemic administration of human cord blood-derived CD34 positive cells to immunocompromised mice subjected to stroke 48 hours early induced neovascularization in the ischemic zone and provided a favorable environment for neuronal regeneration. Endogenous neurogenesis, suppressed by an antiangiogenic agent, is accelerated as a result of enhanced migration of neuronal progenitor cells to the damages area, followed by their maturation and functional recovery.
Our data suggested an essential role for CD34 positive cells in promoting directly or indirectly an environment conducive to neovascularization of ischemic brain so that neuronal regeneration can proceed.
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