| Project/Area Number |
13470282
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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 |
Cerebral neurosurgery
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| Research Institution | Yamagata University |
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Principal Investigator |
KAYAMA Takamasa Yamagata University, School of Medicine, Professor, 医学部, 教授 (50142972)
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| Co-Investigator(Kenkyū-buntansha) |
GOTO Kaoru Yamagata University, School of Medicine, Professor, 医学部, 教授 (30234975)
TSUCHIYA Daisuke Yamagata University, School of medicine, Assistant, 医学部, 助手 (60312724)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥8,500,000 (Direct Cost: ¥8,500,000)
Fiscal Year 2003: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2002: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2001: ¥3,700,000 (Direct Cost: ¥3,700,000)
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| Keywords | neurogenesis / SOD / neural stem cell / free radical / focal cerebral ischemia / cerebral cortex / old age / 老化 |
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| Research Abstract |
1. Cortical neurogenesis in periinfarcted zone and proliferation of neural progenitors in subventricular zone (SVZ) and dentate gyrus (DG) following transient focal cerebral ischemia in rats.
Male Sprague-Dawley rats were subjected to 60 minutes middle cerebral artery occlusion (MCAO). Proliferating cells were labeled 5-bromo-2'-deoxyuridine-5'-monophosphate (BrdU) by cumulative administration before sacrificing animals at 1,2,3,4,6, and 8weeks after ischemia. For the evaluation of cell specificity, NeuN, GFAP and IB4 immunolabeling were performed. In cerebral cortex of periinfarcted zone, we demonstrated BrdU positive cells co-express mature neuronal marker NeuN from 3weeks to 8weeks after ischemia. On the other hand, we observed increasing BrdU positive cells in DG and SVZ of bilateral hemisphere after ischemia. We reported cortical neurogenesis and proliferation of neural progenitors in SVZ and DG following transient focal cerebral ischemia in rats. Since cortical neurogenesis is still controversial, we need to do further investigation to disclose the actual condition of neurogenesis.
2. SOD1 overexpressing mice exhibit preservation of neural stem cells in aging and increase of neural stem cells following focal cerebral ischemia.
We investigated the correlation between SOD1 and the proliferation of neural stem cells in aging as chronic oxidative stress (study 1) and acute oxidative stress induced by transient focal cerebral ischemia (study 2) in these mice. In study 1, 16-month-old transgenic mice showed a significant increase of neural stem cells in the SVZ compared with wild-type (p=0.0001). In study 2, mice were subjected to 30 min MCAO. The increase of neural stem cells in the DG in transgenic mice was significantly greater than that in wild-type (p<0.05). Our results suggest that chronic and acute oxidative stress may inhibit the proliferation of neural stem cells and that SOD1 may play a key role in their proliferation.
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