2011 Fiscal Year Final Research Report
Investigation of role of glial cells in glaucomatous optic neuropathy and searching glial cell-related treatment for glaucoma
| Project/Area Number |
21592220
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | University of Yamanashi |
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Principal Investigator |
KASHIWAGI Kenji 山梨大学, 大学院・医学工学総合研究部, 准教授 (30194723)
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| Co-Investigator(Kenkyū-buntansha) |
MABUCHI Fumihiko 山梨大学, 大学院・医学工学総合研究部, 助教 (20322125)
CHIBA Tatsuya 山梨大学, 大学院・医学工学総合研究部, 助教 (50402061)
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| Project Period (FY) |
2009 – 2011
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| Keywords | 緑内障 / グルタミン酸 / グルタミン酸トランスポーター / 眼グリア細胞 / 網膜神経節細胞 / 遺伝子改変マウス |
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| Research Abstract |
I clarified the following points ; Different glutamate transporters(GLT) were differently involved in glial cell-related effect on RGC. Major GLT, GLAST exerted neuroprotective effect on RGC, while GLT-1 exerted effect on promoting neuritis. Muller cells, major retinal glial cells, showed a protective effect on retinal ganglion cells(RGCs), while astrocytes in optic nerve did promoting effect of neurites. Several mRNAs influenced to RGC survival or neurite elongation were identified as key mRNAs for GLT-involved RGC effects. EGFR, Gabbr2, Agtr1a showed protective effect, while Id3、Egr1, Gja1p, App, Nr2f2 mRNAs were involved in RGC death. I developed an animal model that enables to observe axonal flow of lived rat retina.
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