| Project/Area Number |
16K20311
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Ophthalmology
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| Research Institution | University of Fukui |
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Principal Investigator |
Miyake Seiji 福井大学, 学術研究院医学系部門, 助教 (50572765)
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| Research Collaborator |
INATANI MASARU
OKI MASAYA
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 網膜神経節細胞 / 軸索輸送 / ミトコンドリア / 酸性顆粒 / 緑内障 / 酸化ストレス / サイトカイン / 軸索障害 / オートファジー / 細胞死 / オルガネラ |
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| Outline of Final Research Achievements |
In this study, effect of external stimulation of several stresses such as oxidative stress, cytokines, and excitatory amino acid on dynamics of axonal transport of retinal ganglion cells was evaluated. TNF-α and hydrogen peroxide caused axonal shortening and decline in number of mobile mitochondria, however, cell death was not induced by these stimulations in this experimental condition. On the other hands, NMDA and IL-6 had no effect on axonal dynamics and cell viability. Previous our study revealed that depression of axonal transport activity occurred prior to cell death. These data suggested cytokine and oxidative stress were contribute to the risk for progression of glaucomatous optic neuropathy, regardless of ocular pressure.
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| Academic Significance and Societal Importance of the Research Achievements |
緑内障治療のポイントは網膜神経節細胞の消失を少しでも遅らせることである。しかし、手術や点眼を行っても患者によって得られる効果が一定ではないことから、医療現場ではこれまでとは異なるアプローチの治療法が強く望まれている。研究代表者が進める神経保護を指向した緑内障治療法の開発は、治療戦略の幅を広げることができ、視覚障害から生じる総合的なコストを減ずるための方策を、眼圧下降とは異なる視点から提案できる。
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