2015 Fiscal Year Final Research Report
Role of bone metabolism caused by mechanical stress in SHIP KO mice
Project/Area Number |
24593099
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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 |
Orthodontic/Pediatric dentistry
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Research Institution | Nagasaki University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
KITAURA Hideki 東北大学, 歯学研究科(研究院), 准教授 (60295087)
HOTOKEZAKA Hitoshi 長崎大学, 医歯薬学総合研究科(歯学系), 准教授 (90199513)
FUJIMURA Yuji 長崎大学, 医歯薬学総合研究科(歯学系), 助教 (70448504)
|
Project Period (FY) |
2012-04-01 – 2016-03-31
|
Keywords | SHIP / TNF-α / 破骨細胞 / 矯正 |
Outline of Final Research Achievements |
SHIP (SH2-containing inositol-5'-phosphatase) plays an important role for signal transduction of B cell receptor in immunoreaction. In bone metabolism, closely associated with immunology, SHIP also has been researched in recent years. We showed that SHIP might negatively regulate TNF-α mediated osteoclastogenesis in vitro. We also investigated the effect of SHIP caused by methanical stress using an orthodontic tooth movement model in vivo. The amount of tooth movement in SHIP knockout mice wasn’t significantly increased compared with control mice.
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Free Research Field |
矯正
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