2013 Fiscal Year Final Research Report
DNA damage response in development of glaucoma
| Project/Area Number |
23592553
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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 | The University of Tokyo |
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Principal Investigator |
KATSURA Mari 東京大学, アイソトープ総合センター, 特任助教 (30436571)
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| Co-Investigator(Kenkyū-buntansha) |
AIHARA Makoto 東京大学, 医学部附属病院, 准教授 (80222462)
MURATA Hiroshi 東京大学, 医学部附属病院, 助教 (80635748)
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| Project Period (FY) |
2011 – 2013
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| Keywords | DNA損傷応答 / 緑内障 / γ-H2AX / 53BP1 / ヒストンH4K20メチル化 / ラタノプロスト / 視神経保護 / アポトーシス |
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| Research Abstract |
DNA damage response (DDR) includes DNA repair, cell cycle checkpoint and apoptosis. In this study, we showed that under hypoxia, some DDR molecules were involved in retinal ganglion cell (RGC) death. 53BP1, ATM, NF-kB and mono-methylation of histone H4K20 coordinate primary cultured rat RGC survival in cultured RGC. 53BP1 nuclear foci were decreased in rat optic nerve crush model. Prostaglandin F2 alpha analog latanoprost prevents RGC death under hypoxia with mono-methylation of histone H4K20 and 53BP1 nuclear foci. The findings will be useful in development of new therapy for glaucomatous optic neuropathy.
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Research Products
(14 results)
