| Project/Area Number |
24659661
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Hokkaido University |
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Principal Investigator |
IWASAKI Norimasa 北海道大学, 医学(系)研究科(研究院), 教授 (30322803)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAHATA Masahiko 北海道大学, 北海道大学病院, 講師 (40374368)
ONODERA Tomohiro 北海道大学, 大学院医学研究科, 助教 (70547174)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 骨・軟骨代謝学 / スフィンゴ糖脂質 / ガングリオシド / 遺伝子改変マウス / 軟骨 / 骨 / 変形性関節症 / 骨折 / 骨・軟骨代謝 / 糖脂質 |
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| Research Abstract |
Glycosphingolipids (GSLs) are ubiquitous membrane components that modulate transmembrane signaling and mediate cell-to-cell and cell-to-matrix interactions. The purpose of this study was to clarify the functional roles of GSLs in maintaining osteochondral homeostasis using different strains of GSLs synthase knockout (KO) mice. Although all strains of KO mice developed and grew normally, osteoarthritic changes were dramatically enhanced with aging. IL-1 stimulation of chondrocytes from KO mice significantly increased MMP-13 mRNA expression and apoptosis. In addition, KO mice delayed enchondral ossification during fracture repair process. These findings indicate that GSLs have a chondro-/osteo- protective role and prevent disease progression, although GSLs are not essential for osteochondral tissue development in young mice.
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