| Project/Area Number |
23791983
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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 | Kobe University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 眼生化学 / 分子生物学 / 軸索輸送 / 軸索障害 / 該当無し |
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| Research Abstract |
We investigated the expression of syntaphilin in the rat retina, optic nerve and brain. The expression of syntaphilin had a various pattern in the visual system; syntaphilin was occasionally expressed at astrocytes, axons and retinal ganglion cells in the retina, and at cell bodies of neurons in the superior colliculus, while syntaphilin was abundant in the astrocytes of rat optic nerve, which was confirmed by human optic nerve. After optic nerve transection which caused RGC death and axonal degeneration, the gene expression change by quantitative real-time RT-PCR in rat retina and optic nerve was evaluated. Syntaphilin gene and protein expression in optic nerve was down-regulated at 3 and 7 days after optic nerve transection. Our study suggested that syntaphilin in astrocyte at the optic nerve might be involved in axonal injury. Furthermore, we reported axonal loss in human with optic neuropathies including glaucoma using optical coherence tomography.
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