Vascularized peripheral nerve graft and recovery of visual function

2018 Fiscal Year Final Research Report

• Project/Area Number: 15K01400
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Rehabilitation science/Welfare engineering
• Research Institution: Kansai Medical University
• Principal Investigator: WAKABAYASHI Taketoshi 関西医科大学, 医学部, 非常勤講師 (90302421)
• Co-Investigator(Kenkyū-buntansha): 小阪 淳 国際医療福祉大学, 医学部, 教授 (40243216)
• Research Collaborator: HIRAHARA Yukie (WADA Yukie)
• Project Period (FY): 2015-04-01 – 2019-03-31
• Keywords: 視神経傷害 / 視機能再建

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.

Free Research Field

視覚生物学

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。