Molecular relationship between axonal transported substance and microglia in TNF-α-induced optic neuropathy
| Project/Area Number |
20791285
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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 |
KITAOKA Yasuhsi St.Marianna University School of Medicine, 医学部, 講師 (10367352)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2008: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | TNF-α / 視神経 / Nmnat1 / 緑内障 / マイクログリア / Neurofilament / Trx1 / エストロゲン / BDNF / 網膜神経節細胞 / オリゴデンドロサイト / CREB |
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| Research Abstract |
The levels of Nmnat1 mRNA and protein and of NAD were significantly decreased in the optic nerve but not in the retina in TNF-induced optic neuropathy. Exogenous NAD significantly prevented TNF-induced axonal loss and leaded to the preserved organization of microtubules. The TNF-induced microglial activation was significantly inhibited by NAD treatment. On the other hands, p-CREB and BDNF in oligodendrocytes may serve as a protective moderator for optic nerve axons.
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Report
(3 results)
Research Products
(30 results)
