Elucidation of the pathogenesis of disuse osteoporosis and steroid-induced osteoporosis using Fkbp5 knockout mice

2015 Fiscal Year Final Research Report

• Project/Area Number: 26670811
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Functional basic dentistry
• Research Institution: Nagasaki University
• Principal Investigator: KOMORI Toshihisa 長崎大学, 医歯薬学総合研究科(歯学系), 教授 (00252677)
• Co-Investigator(Renkei-kenkyūsha): MORIISHI Takeshi 長崎大学, 医歯薬学総合研究科(歯学系), 助教 (20380983) ; FUKUYAMA Ryo 広島国際大学, 薬学部, 講師 (20389117)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: グルココルチコイド / ステロイド性骨粗鬆症 / Fkbp5 / 骨細胞 / メカルカルストレス

Outline of Final Research Achievements

We are clarifying the functions of osteocyte network using osteoblast-specific Bcl2 transgenic mice, in which osteocyte network is completely disrupted. We identified Fk506 binding protein 5 (Fkbp5), which was induced in osteoblasts and osteocytes on unloaded condition in the presence of osteocyte network.
Fkbp5 is a chaperon molecule, which binds to steroid receptor. To investigate the functions of Fkbp5 in bone, we generated Fkbp5 knockout (Fkbp5-/-) mice. Fkbp5-/- mice showed more severe reductions of bone mass at unloaded condition and in the treatment of glucocorticoid as compared with those in wild-type mice.

Free Research Field

骨代謝学