Msi2 modulates RANKL-induced osteoclastogenesis

• Project/Area Number: 24592256
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Orthopaedic surgery
• 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)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Project Status: Completed (Fiscal Year 2014)
• Budget Amount: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000); Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000); Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000); Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
• 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.