Elucidation of cause of glaucoma by a MAN-network analysis
| Project/Area Number |
23659810
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Ophthalmology
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| Research Institution | University of Yamanashi |
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Principal Investigator |
KOIZUMI Schuichi 山梨大学, 大学院・医学工学総合研究部, 教授 (10280752)
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| Co-Investigator(Kenkyū-buntansha) |
KASHIWAGI Kenji 山梨大学, 医学工学総合研究部, 准教授 (30194723)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 緑内障 / グリア細胞 / ミューラー細胞 / 網膜神経節細胞 / ATP / P2Y6受容体 / RGC / アストロサイト / P2受容体 / 突起伸展 |
|---|
| Research Abstract |
Effects of retinal glial cells (Muller cells and retinal astrocytes) on retinal ganglion neurons (RGCs) were investigated. Retinal glia, by releasing ATP or nucleotides, communicated with RGCs (MAN-network) to elongate the neurites. Responsible P2 receptor and intracellular signal for the elongation was P2Y6 receptor and Akt, respectively. Retinal glia had an important role in regulation of several RGCs’ functions including their elongation etc.
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Report
(3 results)
Research Products
(35 results)
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[Journal Article] Astrocytes 図 5 RGC と視神経グリア細胞の共培養系 (A)共培養系の模式図。視神経グリア細胞由来の液性因子は、半透膜を介して RGC に到達できる。 (B)視神経グリア細胞は、細胞外ATP/UDP 依存的に RGC の突起を伸展させた。 図 4 RGC の P2Y6 受容体 (A)UDP 刺激により惹起される RGC の細胞内Ca2+濃度上昇。(B)UDP 及び ATP により惹起された Ca2+濃度上昇のまとめ。(C)Western blotting による RGC 及びアストロサイトのP2Y6 受容体の確認。 protect neurons against methylmercury via ATP/P2Y_1 receptor-mediated pathways in astrocytes2013
Author(s)
Noguchi, Y., Shinozaki, Y., Fujishita, K., Shibata, K., Imura, Y., Morizawa, Y., Gachet, C. and Koizumi, S.
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Peer Reviewed
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[Book] 眼科2011
Author(s)
柏木賢治
Total Pages
5
Publisher
緑内障手術に関する最近の病態理解
Related Report
