| Project/Area Number |
23500448
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Osaka University |
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Principal Investigator |
INAGAKIS shinobu 大阪大学, 医学(系)研究科(研究院), 教授 (90151571)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUYAMA Tomohiro 兵庫医科大学, 医学部, 教授 (10219529)
FURUYAMA Tatsuo 香川県立保健医療大学, 教養部, 教授 (20238702)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | glia / oligodendrocyte / development / myelin / brain / semaphorin / regeneration / repair / オリゴデンドロサイト / 脳の発達 / 髄鞘形成 / 細胞死 / 脳虚血 / 脳の修復 / 大脳皮質 / セマフォリン / オリゴデンドログリアの分化成熟 |
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| Research Abstract |
Oligodendrocyte (OL) precursor cells (OPCs) that can proliferate and generate OLs, and surve as the primary source of remyelinating cells, are contained in the adult brain. In this study, we showed that Sema4D, found as an axon guidance regulator, plays a role as a negative regulator of OL development. Sema4D-deficiency increased in number of OLs, but not OPCs, suggesting that Sema4D enhances OL survival and promotes OL development. OLs as well as neurons are quite vulnerable to ischemic stress but shows powerful restorative ability after brain injury. Recent studies show that adult brain has the capability to self-repair in response to stroke, suggesting that proliferation and differentiation into myelinating OLs are important in regeneration and repair after brain injury. Sema4D-deficiency enhanced cell proliferation and the number of OLs in the peri-infarct area, suggesting that counteracting inhibitors of Sema4D are possible to improve brain repair in response to cerebral ischemia.
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