| Project/Area Number |
23659716
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Nagoya University |
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Principal Investigator |
HIRAIWA Hideki 名古屋大学, 医学部附属病院, 病院助教 (70566976)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAI Tadahiro 名古屋大学, 大学院・医学系研究科, 講師 (60378198)
HAMADA Takashi 名古屋大学, 大学院・医学系研究科, 助教 (90566978)
YAMAMOTO Ryuichiro 名古屋大学, 大学院・医学系研究科, 医員 (80586743)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 関節病学 / 軟骨代謝 / 加齢 / 変形性膝関節症 / 後期糖化最終生成物 |
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| Research Abstract |
To obtain a novel knowledge about the progression of osteoarthritic knee, we investigated the function of advanced glycation endproducts (AGE) and the receptor of AGE (RAGE) in the process of osteoarthritisusing the cartilage and the meniscus from osteoarthritic knee. The catabolic effects ofmeniscus by AGE were regulated through RAGE pathways, and were suppressed by hyaluronan which is used for treatment of osteoarthritic knee. Moreover, S100 protein, that is one of the ligand of RAGE and secreted by damaged tissues of osteoarthritic knee, regulated the catabolic effects of cartilage via p38 MAPK and NF-kappaB pathways.
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