| Project/Area Number |
22659315
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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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 |
KITAOKA Yasushi 聖マリアンナ医科大学, 医学部, 講師 (10367352)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥3,230,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | 緑内障 / オートファジー / 軸索保護 / LC-3 / Nmnat / TNF / microtubule / neurofilament / kinesin / 網膜神経節細胞 |
|---|
| Research Abstract |
Since mitochondria regulate the multistep process of autophagy, we examined mitochondrial dysfunction in optic nerve. A significant decrease in mitochondrial thioredoxin 2(Trx2) level was observed in the optic nerve after intraocular pressure(IOP) elevation. We also showed the quantification of microtubules and neurofilaments in axon in optic nerve degeneration. LC-3II, which is an autophagy marker, is upregulated in the optic nerve after IOP elevation. Rapamycin, an inducer of autophagy, ameliorated the axonal loss induced by IOP elevation. Thus, these findings suggest the modulation of mitochondria and autophagy as a new treatment strategy for optic nerve degeneration.
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