Ｆｋｂｐ５ノックアウトマウスを用いた不動性・ステロイド性骨粗鬆症発症機構の解明

为了观察废用性骨质疏松症，采用尾部悬吊的方法制作动物模型进行卸载。在生理条件下，FKBP5-/-小鼠的骨体积与野生型小鼠相似。尾部悬吊后，FKBP5-/-小鼠的骨丢失比野生型小鼠更严重。为了检测GC诱导的骨质疏松，在野生型和FKBP5-/-小鼠中植入强的松龙或注射地塞米松。在FKBP5-/-小鼠中，GC处理比野生型小鼠更严重地减少了皮质骨体积和骨形成。这些结果表明，FKBP5在卸载和GC治疗过程中可以抑制骨丢失。

To examine the disuse osteoporosis, tail suspension was used for an animal model for unloading. In physiological condition, the bone volume of Fkbp5-/- mice was similar to that of wild-type mice. After tail suspension, bone loss was more severe in Fkbp5-/- mice than wild-type mice in micro-CT analyses.To examine GC-induced osteoporosis, implantation of prednisolone or injection of Dex was performed in wild-type and Fkbp5-/- mice. The GC treatment reduced cortical bone volume and bone formation more severely in Fkbp5-/- mice than wild-type mice. These finding indicated that Fkbp5 inhibits bone loss in unloading and GC treatment.