| Project/Area Number |
16K20325
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Ophthalmology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
HATANAKA HIROKI 京都府立医科大学, 医学(系)研究科(研究院), 客員講師 (80368050)
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| Research Collaborator |
YONEDA Kazuhito 京都府立医科大学, 医学(系)研究科(研究院), 助教 (00347460)
Yamagishi Tetsuya 京都府立医科大学, 医学部附属病院, 助教 (40733572)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 線維化 / epigenesis / HDAC / CNV / AMD / 眼内線維化 / epigenetic / HAT / 眼科学 / 眼生化学 / 分子生物学 |
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| Outline of Final Research Achievements |
Age-related macular degeneration (AMD) is the major cause of vision loss and poor visual prognosis due to the chorioretinal fibrosis. Recent studies indicated that histone deacetylase (HDAC) activity is also associated with the development and progression of some chronic diseases characterized by the accompanied fibrosis. To investigate the effects of a new HDAC inhibitor, OBP801, on RPE fibrosis and neovascularization, the integral gene expression analysis in cultured human RPE cells was performed and the reduced laser-induced choroidal neovascularization (CNV) was confirmed in murine models. OBP801 suppressed efficiently the expression of diverse genes which relating with fibrosis, CNV and tissue scarring. OBP801 did reduce the area of laser-induced fibrosis and choroidal neovascularization lesions. The findings will help developing the new treatment modalities against AMD, specifically targeting the fibrosis.
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