| Project/Area Number |
22591694
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Kinki University |
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Principal Investigator |
AKAGI Masao 近畿大学, 医学部, 教授 (00273441)
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| Co-Investigator(Kenkyū-buntansha) |
ASADA Shigeki 近畿大学, 医学部, 講師 (00330283)
HASHIMOTO Kazuhiko 近畿大学, 医学部附属病院, 助教 (10635569)
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| Co-Investigator(Renkei-kenkyūsha) |
SAWAMURA Tatsuya 国立循環器病センター(研究所), 脈管整理部, 部長 (30243033)
TERAMURA Takeshi 近畿大学, 医学部, 医学部講師 (40460901)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 医療・福祉 / 細胞・組織 / 脂質 / トランスレーショナルリサーチ / 老化 / 細胞・細胞 / トランスレーショナルリサ |
|---|
| Research Abstract |
Purpose of this study is to demonstrate involvement of the ox-LDL/LOX-1 system to joint cartilage degeneration in vivo using LOX-1 knockout (KO) mouse. To develop a nonsurgical murine knee osteoarthritis model, mechanical load is applied by forced running on a treadmill, which was controlled by changing number of forced running periods and running time. Changes in the degeneration score increased significantly in a time- and dose-dependent manner. However, LOX-1 KO did not show significant protective effects in this OA model after 2-week forced running, compared with wild type mice. While, long-term observation (1 and 1.5 year) of the KO mice and wild type mice bred conventionally in cages revealed significant difference in cartilage degeneration. Furthermore, LOX-1 KO suppressed synovitis and cartilage degeneration in zymosan induced arthritis. These results indicate that the ox-LDL/LOX-1 system is involved to joint cartilage degeneration in vivo. In conclusion, the ox-LDL/LOX-1 system may play some role not only in endothelial dysfunction of atherosclerosis but also in cartilage degeneration.
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