| Project/Area Number |
25461628
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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 |
Pediatrics
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
Hamaoka Kenji 京都府立医科大学, 医学(系)研究科(研究院), 教授 (60189602)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Akihiro 京都府立医科大学, 大学院医学(系)研究科(研究院), 博士研究員 (50313854)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | mannose binding lectin / vasculitis / Kawasaki disease / mouse model / complement / 川崎病 / MASPs / MBL / C1INH / Mannose binding lectin / 血管炎 / 自然自己抗体 / MASP / 川崎病動物モデル |
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| Outline of Final Research Achievements |
Kawasaki disease (KD) is an idiopathic vasculitis. Its etiology is not clear, some clinical genetic studies have indicated involvement of genetic polymorphisms of mannose binding lectin (MBL) gene in the disease. Using an animal model for KD, in this study, we explored the roles of MBL in KD. Deposition of MBL-A, MBL-C and complement were observed in the aortic root including coronary arteries in the model mice. Plasma MBL-A lebel was gradually increased with development of the vasculitis, whereas plasma MBL-C level was rapidly decreased. Employing proteomics , forthermore, we revealed that MBL-A and -C interact with some specific endogenous proteins to activate lecin pathway in vitro weakly but significantly.
Taken together, these results suggest that MBLs involve in exacerbration of KD-like murine vasculitis through interacting with intracellular proteins released from damaged tissues.
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