| Project/Area Number |
24791507
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Osaka University (2013)
Ehime University (2012) |
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Principal Investigator |
SUGIMOTO Kana 大阪大学, 医学(系)研究科(研究院), 助教 (00581034)
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| Co-Investigator(Renkei-kenkyūsha) |
TANAKA Junya 愛媛大学, 大学院・医学系研究科, 教授 (70217040)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 脳梗塞 / NG2コンドロイチン硫酸プロテオグリカン / マイクログリア / TGF-β1 / TGFβ1 |
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| Research Abstract |
We investigated activated microglia in ischemic brain lesions. Activated microglia expressing NG2 chondroitin sulfate proteoglycan (NG2) were found only in the narrow zone (demarcation zone) that demarcated the peri-infarct tissue and ischemic core. NG2(+) microglia expressed both CD68 and a TREM-2, suggesting that NG2(+) microglia eliminated apoptotic neurons. In fact, NG2(+) microglia often attached to degenerating neurons and sometimes internalized NeuN(+) or neurofilament protein(+) material.Kinetic studies revealed that expression of transforming growth factor (TGF)-beta1 was most evident in the ischemic core. In response to TGF-beta1, primary microglia enhanced the expression of NG2 protein and TREM-2 mRNA as well as migratory activity.A TGF-beta1 inhibitor, SB525334, abolished these effects. The present results suggest that TGF-beta1 produced in the ischemic core diffused toward the peri-infarct tissue, driving activated microglial cells to eliminate degenerating neurons.
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