| Project/Area Number |
23500489
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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 |
Laboratory animal science
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| Research Institution | Tokyo University of Science (2012-2013)
The University of Tokyo (2011) |
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Principal Investigator |
KAIFU Tomonori 東京理科大学, 生命医科学研究所, 助教 (90343037)
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| Co-Investigator(Kenkyū-buntansha) |
IWAKURA Yoichiro 東京理科大学, 生命医科学研究所, 教授 (10089120)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | C型レクチン受容体 / サイトカイン / 骨代謝 |
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| Research Abstract |
Ankylosing spondylolysis (AS) is one of typical diseases in spondyloarthlopathy, which develops ankylosis in joints, such as the spines and the sacroiliacs. Although enthesitis, an inflammation of the entheses, is known as a primitive symptom of ankylosisng spondylitis, the pathogenesis remains unclear and the curative treatment isn't yet determined. Since DCIR deficient mice spontaneously developed enthesitis and ankylosing in ankles, we exploited the DCIR deficient mice to understand the pathogenesis of an inflammation in the enthuses and a subsequent ankylosis as well as to generate a new animal mode for analyzing AS. We found that a pro-inflammtory cytokine was implicated in the development of ankylosis, which had the ability to facilitate bone formation. Therefore, this study demonstrates that the DCIR deficient mice are a useful animal model of AS to analyze the pathogenesis and to assess a potential reagent to cure the disease.
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