Estabilish of new molecular mechanism in retinal ganglion cell degeneration.
| Project/Area Number |
25462739
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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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 |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 網膜 / 緑内障 / 視神経 / 細胞死 / TLR-4 / アポトーシス |
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| Outline of Final Research Achievements |
The purpose of this study is to investigate the neurotoxicity of HistoneH2B(H2B) through TLR4 in the mice retina. iIVI of 300 µmol H2B on wild mice showed significant RGC loss compared with the control. IVI of H2B on TLR4-/- mice did not show RGC loss compared to wild mice.
Dramatic upregulation of inflammatory cytokines mRNA was observed in the retina after IVI of H2B, suppression of these changes was observed in TLR4-/- mice (IL-1β; wild 118.0 TLR4-/- 22.4 fold/control, TNF α; wild 37.7 TLR4-/- 3.4, TGF-β; wild 3.1 TLR4-/- 1.1). Furthermore, significant phosphorylation of JNK and P38 was observed in wild mice, in contrast, no obvious phosphorylation of these proteins was observed in TLR4-/- mice.
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Report
(4 results)
Research Products
(10 results)
