| Project/Area Number |
26462291
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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 |
Orthopaedic surgery
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
Imai Shinji 滋賀医科大学, 医学部, 教授 (90283556)
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| Co-Investigator(Kenkyū-buntansha) |
松末 吉隆 滋賀医科大学, 医学部, 副学長 (30209548)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 力学的骨形成調節 / 骨芽細胞 / 骨細胞 / pleiotrophin |
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| Outline of Final Research Achievements |
In agreement with previous reports, the skeletal structure of the PTN knockout mice developed normally. However, a subtle growth retardation of the weight-bearing bones was observed upon adulthood, suggesting a link to physical activity. Adult PTN deficient mice were characterized by low turnover and osteopenia, as well as resistance to exercise/immobilization-dependent bone remodeling. PTN was localized around osteocytes and their processes in vivo and furthermore, osteocytic PTN expression was upregulated by mechanical loading in vitro. PTN did not have any effect on human osteoclast formation or resorption in vitro. Our results suggest that PTN is an osteocyte-derived factor that can mediate the osteogenic effects of mechanical loading on bone. Thus, PTN could be a novel promising target to enhance bone maintenance and regeneration.
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