2014 Fiscal Year Final Research Report
Msi2 modulates RANKL-induced osteoclastogenesis
Project/Area Number |
24592256
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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 | The University of Tokyo |
Principal Investigator |
KADONO Yuho 東京大学, 医学部附属病院, 講師 (70401065)
|
Co-Investigator(Kenkyū-buntansha) |
YASUI Tetsuro 東京大学, 医学部附属病院, 講師 (30583108)
OSHIMA Yasushi 東京大学, 医学部附属病院, 講師 (50570016)
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | 破骨細胞 / 分化 / RANKL |
Outline of Final Research Achievements |
We generated osteoclasts in vitro by stimulating BMMs with RANKL and M-CSF and performed quantitative RT-PCR and immunoblotting to evaluate Msi2 expression during osteoclastogenesis. Msi2 gene and protein expression were upregulated by RANKL stimulation. Cells collected from Msi2-deleted mice formed fewer oseteoclasts by RANKL stimulation than wild type. Micro-CT analysis revealed that there is no significant difference in bone volume between wild type mice and Msi2-deleted mice. However, difference of bone volume between sham and ovariectomized Msi2-deleted mice was higher than wild type mice.
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Free Research Field |
骨代謝
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