| Project/Area Number |
23591445
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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 |
膠原病・アレルギー・感染症内科学
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
KOHNO Masataka 京都府立医科大学, 医学(系)研究科(研究院), 助教 (60405256)
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| Co-Investigator(Kenkyū-buntansha) |
NAKADA Hiroshi 京都産業大学, 公私立大学の部局等, 教授 (90113141)
KAWAHITO Yutaka 京都府立医科大学, 医学(系)研究科, 准教授 (50336731)
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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 |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | スフィンゴシン１リン酸 / S1P3 / コラーゲン誘導関節炎 / 炎症 / 関節リウマチ / スフィンゴシン1リン酸（S1P） / S1P3レセプター / コラーゲン誘導関節炎(CIA) / スフィンゴシン1リン酸 |
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| Research Abstract |
It is suggested that S1P is an important inflammatory mediator in the pathogenesis of arthiritis, but the role of S1P3 in it is poorly understood. Thus, we examined the role of S1P3 receptor signaling in the development of collagen-induced arthritis (CIA) in murine.
S1P3-/- mice showed signiflcantIy lower arthritis severity score compared with wild type(WT) mice (P < 0.05, Mann-Whitney U test). Histopathological evaluation of paws obtained on the 42nd day showed marked reductions in synovial inflammation and bone erosion parameters in S1P3-/- mice compared with WT mice (P < 0.05). Serum anti-type II collagen antibodies were not satatistically different between WT and S1P3-/- mice. These results indicate that S1P3 receptor signaling plays an important role in the development of murine collagen-induced arthritis model. Also it is suggested that S1P-S1P3 signaling is a new therapeautic target for rheumatoid arthritis.
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