| Project/Area Number |
15K01400
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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 |
Rehabilitation science/Welfare engineering
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| Research Institution | Kansai Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
小阪 淳 国際医療福祉大学, 医学部, 教授 (40243216)
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| Research Collaborator |
HIRAHARA Yukie (WADA Yukie)
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 視神経傷害 / 視機能再建 / 網膜神経節細胞 / 網膜脂質構成 / 神経細胞死 / 軸索再生 / 細胞膜 / 血管柄付き末梢神経移植 |
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| Outline of Final Research Achievements |
We have reviled the axonal regeneration of retinal ganglion cells (RGC) is induced by autologous peripheral nerve graft, and the efficient approach to regenerate of axon needed the environment adjustment of RGC. However, it remains unknown about the RGC environment by optic nerve injury. Thus we analyzed molecular alteration of retina after traumatic optic nerve injury (TONI), especially the major lipid component of cell membrane. Phosphatidylinositol (PI) 18:0/20:6 was localized to the three nuclear layer structures in control retina, but the localization of 18:0/20:6 PI after TONI was decreased in the outer nuclear layer. Meanwhile, phosphatidylserine (PS) 18:0/22:6 specifically showed in the inner plexiform layer, but the signal intensity was dramatically reduced after TONI. Phosphatidylethanolamine (PE) with docosahexaenoic acid was increased after TONI. These results suggest that not only RGC but also other retinal neurons were influenced by TONI.
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| Academic Significance and Societal Importance of the Research Achievements |
従来の光学顕微鏡レベルの研究で、視神経傷害後にはRGCとグリア細胞の分子発現が変化することは知られていた。一方で、視神経切断は視細胞など他のニューロンには影響しないとされていた。しかし今回の報告により、視神経傷害は視神経に軸索を投射しているRGCだけでなく、網膜全層にわたって分子レベルの変化を引き起こし、RGCの細胞死や軸索再生に影響を及ぼしていることが示唆された。このことは、RGCの生存・軸索再生、さらには末梢神経移植により視機能再建を目指すうえでRGC以外のニューロンの機能変化も考慮する必要があることを明らかにした点で、学術的に極めて重要な知見である。
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