The clarification of the role of Mpp7 in bone tissue

Research Project

Project/Area Number	18K09057
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Review Section	Basic Section 56020:Orthopedics-related
Research Institution	Niigata University
Principal Investigator	Kondo Naoki 新潟大学, 医歯学総合病院, 講師 (70543388)
Project Period (FY)	2018-04-01 – 2021-03-31
Project Status	Completed (Fiscal Year 2020)
Budget Amount *help	¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000) Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000) Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000) Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Keywords	Mpp7遺伝子 / 体重 / ノックアウトマウス / 骨密度 / Mpp 7 / 骨粗鬆症 / 骨密度決定候補遺伝子 / MPP-7 / Mpp7 / 骨芽細胞 / 破骨細胞
Outline of Final Research Achievements	Osteoporosis is main risk factor of fragility fractures and results in lower quality of life. Human genome wide associated analysis clarified that membrane palmitoylated protein 7(MPP7) gene is significantly associated with bone mineral density (BMD). The lower expression level in MPP7, the lower in BMD. We established MPP7 general knockout mice and analyzed the function of MPP7 in vivo. Statistically significant body weight loss was detected in female MPP7 knockout mice than in female wild type mice, but not in male MPP7 knock out mice. Except body weight, no difference such as bone histology, growth plate thickness was detected. In addition, MPP7 protein was expressed in several human osteosarcoma cell lines.
Academic Significance and Societal Importance of the Research Achievements	MPP7が生体内において体重制御に関与すること、樹立したMPP7欠損マウスがMPP7による骨密度の制御機構を解析する上で、有用なモデル動物になることを示した。 HTLV-1は成人T細胞白血病およびHTLV-1関連脊髄症の原因ウイルスである。これらの病気の発症には、HTLV-1のTax蛋白が深く関与する。MPP7およびDLG1をTaxの結合因子として同定した。HTLV-1の病原性におけるMPP7の役割は不明であり、Mpp7-floxマウスおよびMpp7-KOマウスはHTLV-1の病原性を解析する有用なツールになる。