| Project/Area Number |
21791718
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Ophthalmology
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| Research Institution | St.Marianna University School of Medicine |
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Principal Investigator |
MUNEMASA Yasunari St.Marianna University School of Medicine, 医学部, 助教 (30440340)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 緑内障 / ミトコンドリア / 軸索変性 / 網膜神経節細胞死 / Thioredoxin2 / AIF / 酸化ストレス / TNF-α / TNF-a |
|---|
| Research Abstract |
A decrease in Mitotracker labeled mitochondria around lamina area at the optic nerve was observed in glaucomatous eye. Significant decrease in thioredoxin2 (Trx2) level was observed in the glaucomatous mitochondria. The change of mitochondrial apoptosis-inducing factor (AIF) was slightly decreased, whereas significant increase in axoplasmic AIF was observed in the glaucomatous optic nerve. Furthermore, substantial increase in nucleus AIF was observed in RGCs after IOP elevation. Thus, a decreased mitochondrial membrane potential and subsequent AIF translocation were involved in glaucomatous neurodegeneration. Furthermore, modulation of mitochondria through the inhibition of AIF translocation may become new strategy for neurodegenerative disease, such as glaucoma.
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