2015 Fiscal Year Final Research Report
Osteoclast-derived factors for inhibiting sclerostin expression is a bone coupling factor.
| Project/Area Number |
25670792
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Functional basic dentistry
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| Research Institution | Matsumoto Dental University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KOIDE Masanori 松本歯科大学, 総合歯科医学研究所, 講師 (10367617)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | スクレロスチン / 破骨細胞 |
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| Outline of Final Research Achievements |
Bone remodeling is achieved by the cooperation of bone forming osteoblasts, bone resorbing osteoclasts, and matrix-embedded osteocytes. Sclerostin (Sost) secreted from osteocytes inhibits the Wnt / β- catenin signaling, which in turn, suppresses bone formation. OPG-deficient mice (OPG-KO) exhibit increased bone resorption and formation activity. We have found that the expression of Sost is significantly reduced in OPG-KO mice. This finding suggests that the expression of Sost is regulated by factors associated with the increased bone resorption. We also found that culture supernatant collected from osteoclast cultures suppressed the expression of Sost in UMR106 cells. Thus, this study revealed that osteoclasts secrete cytokines X and then suppress the expression of Sost.
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| Free Research Field |
生化学
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