| Project/Area Number |
22591972
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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 | Osaka Medical College |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Tsunehiko 大阪医科大学, 医学部, 教授 (70222891)
OKU Hidehiro 大阪医科大学, 医学部, 准教授 (90177163)
KOJIMA Shota 大阪医科大学, 医学部, 講師 (10388259)
TAKAI Shinji 大阪医科大学, 医学部, 准教授 (80288703)
SHIMAZAWA Masamitsu 岐阜薬科大学, 薬学部, 准教授 (80381721)
KURIMOTO Takuji 大阪医科大学, 医学部, 助教 (50388815)
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| Co-Investigator(Renkei-kenkyūsha) |
HARA Hideaki 岐阜薬科大学, 薬学部, 教授 (20381717)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | P2X7 受容体 / 緑内障 / 視神経挫滅 / 眼圧上昇 / 網膜神経節細胞 / ラット / P2X7受容体 / 急性眼圧上昇モデル / OxATP / BBG / TNF-α / IL-1β / 視神経挫滅モデル / Ox-ATP / p38 / ミクログリア |
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| Research Abstract |
We aimed to determine whether P2X7 receptor is involved in retinal ganglion cell (RGC) loss in rat models of glaucoma. In the first study, we investigated whether P2X7 antagonists rescue RGCs in culture and after optic nerve crush (ONC) injury. In vitro, RGCs were preserved when treated with P2X7 antagonists. In vivo, the retinal expression of the P2X7 receptors was observed to be upregulated after ONC. RGCs were preserved when P2X7 antagonists were applied after ONC injury. In the second study, we evaluated effects of P2X7 antagonists in a rat model of acute intraocular pressure (IOP) elevation. P2X7 receptor was activated after IOP elevation and administration of P2X7 antagonists dose-dependently preserved RGC density. These results suggest that P2X7receptor may be involved in RGC loss in glaucoma models.
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