| Project/Area Number |
25893015
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Ophthalmology
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| Research Institution | Tohoku University |
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Principal Investigator |
FUJITA Kosuke 東北大学, 医学系研究科, 助手 (80708115)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | Glaucoma / Adeno-associated virus / RNAi / 緑内障 / アデノ随伴ウイルス |
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| Outline of Final Research Achievements |
Glaucoma, a leading cause of blindness, is characterized by the progressive loss of retinal ganglion cells (RGCs); however, the molecular component modulated by cell death and the mechanisms of this modulation have not been fully understood.
Recently, our laboratory performed a comprehensive gene expression analysis of the murine retina in the optic nerve crush injury (Yasuda et al., 2014). To identify molecules involved in the RGS cell death signaling characterize their modulation, we conducted RNAi and overexpression experiments using adeno-associated virus. Using mice devoid of Chop and AAV2/2 carrying Chop transgene, we found that RGC death was indeed mediated specifically through Chop signaling, suggesting that ER stress seems to play an important role in the pathogenesis of RGC death following axonal injury, which is in agreement with recent comprehensive gene expression studies.
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