| Project/Area Number |
16K11326
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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 | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Nagata Maho 京都府立医科大学, 医学部附属病院, 客員講師 (40614102)
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| Research Collaborator |
Fullwood Nigel Lancaster University, Research directory
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | RSPO1 / 角膜混濁 / Wnt / 炎症 / 創傷治癒 / 角膜上皮 / S100A8/A9 / カルシウム沈着 / R-spondin1 / タイトジャンクション / S100A8 / S100A9 / 角膜 / Wntシグナル / 眼科学 |
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| Outline of Final Research Achievements |
Corneal transparency is necessary to maintain visual function, but the mechanism to keep its transparency remains unclear. We found that RSPO1 gene-deficient mouse gradually occurs corneal opacity and deposit. In this mouse, increased inflammation and delayed wound healing were found. Moreover, we found that the barrier function of the corneal epithelium was poor in this mouse and the deposits within cornea contained calcium. Gene expression analysis of the corneal epithelium revealed that the calcium-binding proteins S100A8/A9 were remarkably up-regulated in RSPO1 gene-deficient mouse. We suppose that RSPO1 originally keeps the barrier function of corneal epithelium, suppresses S100A8/A9 expression, and prevents accumulating calcium deposits. We conclude that RSPO1 is one of the key to elucidate the mechanism of maintaining the corneal transparency.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は、角膜の透明性維持機構の一部を解明するものである。角膜の透明性が失われる疾患で、とくに炎症が遷延したり創傷治癒遅延がおこる素因があると、角膜移植を行っても最終的に透明性維持が難しく視力が回復しない場合がある。角膜の透明性維持機構を解明することで、今まで治癒することが難しかった角膜疾患の治療に役立てられる可能性がある。本研究では、RSPO1が炎症を制御し創傷治癒を促進することがわかり、同時にカルシウム沈着を主とする角膜混濁を抑制する働きがあることが証明され、角膜の透明維持機構の一部に迫るとともに角膜混濁を生じる疾患の治療への基盤となる知見となった。
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