2017 Fiscal Year Final Research Report
p130Cas is involved in osteocyte's mechanosensory function in bone homeostasis
Project/Area Number |
15K10501
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Orthopaedic surgery
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Research Institution | Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology |
Principal Investigator |
Miyazaki Tsuyoshi 地方独立行政法人東京都健康長寿医療センター(東京都健康長寿医療センター研究所), 東京都健康長寿医療センター研究所, 研究員 (50376480)
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Co-Investigator(Kenkyū-buntansha) |
時村 文秋 地方独立行政法人東京都健康長寿医療センター(東京都健康長寿医療センター研究所), 東京都健康長寿医療センター研究所, 研究員 (80242147)
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Co-Investigator(Renkei-kenkyūsha) |
SAWADA YASUHIRO 国立障害者リハビリテーションセンター(研究所), 研究所 運動機能系障害研究部, 部長 (50313135)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | メカニカルストレス / 骨細胞 |
Outline of Final Research Achievements |
Osteocytes are recognized as mechanosensory cells, although it is largely unknown how bone metabolism is mechanically modulated. Here, we report that p130Cas (Cas) plays a major role in osteocyte mechanosensing to subsequently support bone homeostasis. Osteocyte-specific Cas knockout (Cas cKO) mice exhibit osteopenia. We used a mouse bone-unloading model, in which one of the hindlimbs of each individual mouse was subjected to sciatic and femoral nerve resection. Unloaded femurs exhibited a significant reduction of bone volume as compared with their contralateral controls. Unloaded bones of Casflox/flox mice exhibited significant reduction of bone volume with significantly increased bone resorption parameters. In contrast, bone resorption parameters remained unaltered upon unloading in Cas cKO mice, although they showed a tendency of unloading-induced decrease in bone volume. These results suggest that Cas in osteocytes is involved in the mechanosensory function in bone.
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Free Research Field |
外科系臨床医学・整形外科学
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