| Project/Area Number |
18K09433
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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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| Review Section |
Basic Section 56060:Ophthalmology-related
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| Research Institution | Iwate University |
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Principal Investigator |
Tabata Kitako 岩手大学, 理工学部, 特任准教授 (80714576)
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| Co-Investigator(Kenkyū-buntansha) |
富田 浩史 岩手大学, 理工学部, 教授 (40302088)
菅野 江里子 岩手大学, 理工学部, 准教授 (70375210)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 眼生理学 / 遺伝子治療 / 網膜色素変性症 |
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| Outline of Final Research Achievements |
Some of the green algae class family move forward to sunlight to perform photosynthesis efficiently and they use the photosensitive protein, Channelrhodopsin, to detect light. Our developed mVChR1 modified volvox-derived channelrhodopsin that has a broad range of wavelength sensitivity. The expression of mVChR1 in retinal ganglion cells may recover of blindness. Channelrhodopsin uses a vitamin A derivative, retinal, to receive light. However, there is no report how much content is in the degenerated retina. So, we compared the retinal concentration in normal retina with that in degenerated one. The retinal content in the photoreceptor degenerated retina was lower than normal one. We also investigated the synthesis pathways of retinal by using an RNA-seq analysis and revealed that up-regulations of retinal synthesis related enzyme genes were detected. These results indicated that the increase of Vitamin A possibly contributed on enhancing the mVChR1 function.
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| Academic Significance and Societal Importance of the Research Achievements |
網膜色素変性症は4000～8000人に一人が罹患しており、重篤な場合は失明に至る。原因遺伝子は多数発見されており、未だ確立された治療法が無い。当研究室で開発したmVChR1は、視細胞変性により失明に至った網膜の神経節細胞へ発現させることにより、視力を回復させる可能性がある。mVChR1の光受容に重要な役割を担うのはレチナールであり、視細胞変性後の網膜にmVChR1を発現させると、レチナール合成関連酵素遺伝子および輸送タンパク遺伝子の一部の増加が確認されたが、レチナール量が生来のものより低いことがわかった。このことから遺伝子治療後のビタミンA投与により視機能向上できる可能性が示唆された。
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