| Project/Area Number |
15K10909
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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 | Osaka Medical College |
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Principal Investigator |
Kida Teruyo 大阪医科大学, 医学部, 講師 (90610105)
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| Co-Investigator(Kenkyū-buntansha) |
奥 英弘 大阪医科大学, 医学部, 准教授 (90177163)
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| Research Collaborator |
HORIE Taeko 大阪医科大学, 医学部, 研究助手
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | アクアポリン4 / 糖尿病 / 黄斑浮腫 / ミュラー細胞 / VEGF / TGN-020 / 一酸化窒素 / LSFG-Micro / アクアポリン４ / 網膜血管細胞 |
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| Outline of Final Research Achievements |
Aquaporin 4 (AQP4), a water channel protein, is known to be expressed in retinal Muller cells. The purpose of this study was to determine the effects of VEGF and AQP4 channels on the volumetric changes in Muller cells.
presence or absence of VEGF and TGN-020, a selective AQP4 inhibitor.
In the diabetic rat retina, VEGF immunoreactivity was concentrated in the internal retinal layers, and AQP4 immunoreactivity was higher than controls. The expressions of AQP4 were colocalized with GFAP. Protein levels of VEGF in the hyperglycemic rat retina were significantly higher than controls. FACS analyses showed that exposure to VEGF enlarged Muller cells, while exposure to TGN-020 suppressed the enlargement. Intracellular levels of NO were increased after exposure to VEGF, which was suppressed following the addition of TGN-020. The observed Muller cell swelling is mediated by VEGF and AQP4.
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