| Project/Area Number |
18K15367
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 51030:Pathophysiologic neuroscience-related
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| Research Institution | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 神経回路修復 / 延髄錐体切断 / RNA-seq / ミクログリア / アストロサイト / 免疫 / 脊髄 / 神経再生 |
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| Outline of Final Research Achievements |
After central nervous system injury, compensatory neural circuit is formed, and neural function is partially recovered. This ability is higher in neonate compared to adult. To explore the factors that initiate the sprouting, and to elucidate the difference of initial response after central nervous system injury between neonate and adult, we extracted RNA from cervical cord of neonatal or adult mice 3 days after pyramidotomy, and performed RNA-sequencing. Inflammatory related genes such as Ccl6 or Cd52 are upregulated in adult after pyramidotomy compared to sham group or neonatal group. The inflammatory related genes are expressed in microglia in denervated side of dorsal column in adult mice, whereas no microglial accumulation is observed in neonatal mice. It is possible that severe inflammatory response in microglia is related to low sprouting ability in adult. The above research is published in BMC Genomics.
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| Academic Significance and Societal Importance of the Research Achievements |
新生児と成体の神経回路修復能の差を規定する要因を解明することは、中枢神経系損傷後の新規治療法につながる可能性があり、重要な課題である。本研究は上記解析の基盤となる遺伝子発現プロファイルを明らかにしたという意義がある。損傷部から離れた部位での過剰な炎症反応が神経回路修復に悪影響を与える可能性や、まだほとんど機能を解析されていない遺伝子Etnpplが新生児と成体で大きく異なる発現を示すことも今回明らかとなった。今後これらの解析を進めることで、冒頭の課題の解明につながることが期待される。
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