| Project/Area Number |
23500422
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | Tokyo Metropolitan Institute of Medical Science |
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Principal Investigator |
KAWANO Hitoshi 公益財団法人東京都医学総合研究所, 脳発達・神経再生研究分野, 研究員 (20161341)
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| Co-Investigator(Kenkyū-buntansha) |
KURODA Junko 公益財団法人東京都医学総合研究所, 脳発達・神経再生研究分野, 研究員 (20142151)
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 神経再生 / 線維性瘢痕 / TGF-beta / コンドロイチン硫酸 / デルマタン硫酸 / TGF-β1 / PDGF / 脳損傷 / TGF-β / プロテオグリカン / 損傷 / グリア瘢痕 |
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| Outline of Final Research Achievements |
The role of chondroitin sulfate (CS) and dermatan sulfate (DS) was examined in mice after transection of nigrostriatal dopaminergic pathway and treatment with of glycosaminoglycan degrading enzymes. Two weeks after injury, fibrotic and glial scars were formed around the lesion and transected axons did not regenerate beyond the lesion. Injection of chondroitinase B. which degrades DS, into the lesion site completely suppressed the fibrotic scar formation, reduced the glial scar and promoted the regeneration of dopaminergic axons. In contrast, injection of chondroitinase AC, a CS-degrading enzyme, did not suppress the fibrotic scar formation, but promoted the axonal regeneration. These results first demonstrate that DS and CS play different functions after CNS injury: DS is involved in the lesion scar formation and CS inhibits axonal regeneration (Li et al., 2013).
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