Project/Area Number |
15K10485
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Orthopaedic surgery
|
Research Institution | University of Miyazaki |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
帖佐 悦男 宮崎大学, 医学部, 教授 (00236837)
黒木 修司 宮崎大学, 医学部, その他 (40418843)
関本 朝久 宮崎大学, 医学部, 講師 (60305000)
荒木 正健 熊本大学, 生命資源研究・支援センター, 准教授 (80271609)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | ラミンBレセプター / 癒合指 / 骨芽細胞 / グリーンバーグ骨異形成症 / 成長障害 / Lbr / 骨代謝 / 軟骨代謝 |
Outline of Final Research Achievements |
Mutation in Lamin B Receptor (LBR) is known to cause severe bone disorders disease, Greenberg dysplasia. Therefore, phenotypic analysis of Lbr trap mice and function analysis of Lbr in osteochondral metabolism were performed. Lbr trap mice showed growth disorder, decreased hair growth, and ichthyosis. Syndactyly were observed as a characteristic phenotype of the skeletal system. No obvious short limb symptoms observed in Greenberg dysplasia were observed. Bone phenotype analysis showed decreased bone strength and bone density. Lamin B Receptor is likely to be involved in bone metabolism, and Lbr trap mice are potential to be model mice of syndactyly.
|