| Project/Area Number |
26893100
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Ophthalmology
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| Research Institution | University of Fukui |
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Principal Investigator |
Seiji Miyake 福井大学, 医学部, 助教 (50572765)
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| Research Collaborator |
INATANI Masaru 福井大学, 医学部, 教授 (40335245)
TAKIHARA Yuji 福井大学, 医学部附属病院, 助教 (50640140)
YOKOTA Satoshi 京都大学, 医学研究科, 大学院生
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| Project Period (FY) |
2014-08-29 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 緑内障 / 網膜神経節細胞 / 軸索輸送 / 細胞小器官 / サイトカイン / 酸化ストレス / ミトコンドリア / 細胞死 / ライブイメージング |
|---|
| Outline of Final Research Achievements |
The pathologies of glaucomatous optic neuropath are cell death of retinal ganglion cells (RGCs) and degeneration of their axons. Recently it is proposed that dysfunction of axonal transport was occurred before the RGC death. In fact, our group confirmed that dysfunction of axonal transport activity, which was induced by microtubule depolymerization and axotomy, is followed by cell death. However, relationship of cellular stresses and dynamics of axonal transport is unknown. In this study, effect of cytokines, which involves in glaucomatous neurodegeneration, and oxidative stress on axonal transport was evaluated in living RGCs.
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