Role of Wnt-Ror2 signals in ruffled border formation in osteoclasts

Wnt-Ror2 信号在破骨细胞皱褶边界形成中的作用

• 批准号: 22659339
• 负责人: TAKAHASHI Naoyuki
• 金额: $ 2.04万
• 依托单位: Matsumoto Dental University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Challenging Exploratory Research
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22659339/
• 关键词: 口腔生化学; 破骨細胞; Wnt非古典経路; 極性化; 波上縁; Wnt5a-Ror2シグナル; 低分子量Gタンパク質; Wnt; Rho; 口腔生化学; 破骨細胞; Wnt非古典経路; 極性化; 波上縁; Wnt5a-Ror2シグナル; 低分子量Gタンパク質; Wnt; Rho

The role of Wnt5a-Ror2 signals in osteoclast function was studied. (1) Bone-resorbing activities of osteoclasts derived from Wnt5a-deficient mice and from Ror2 deficient mice were lower than that of wild-type(WT) osteoclasts. (2) Wnt5a activated Rho, a small G protein, in WT osteoclasts but not in Ror2-deficient osteoclasts. (3) When active Rho was transfected into Ror2-deficient osteoclasts, the bone-resorbing activity was recovered. Thus, Wnt5a-Ror2 signals play important roles in osteoclast function through a Rho-dependent mechanism.

研究了WNT5A-ROR2信号在破骨细胞功能中的作用。 （1）源自Wnt5a缺陷小鼠和ROR2缺乏小鼠的破骨细胞的骨骼抑制活性低于野生型（WT）破骨细胞。 （2）Wnt5a在WT破骨细胞中激活了一种小的G蛋白Rho，但在ROR2缺乏的破骨细胞中没有激活Rho。 （3）当主动Rho转染到ROR2缺陷骨细胞中时，恢复了骨呈现活性。因此，Wnt5A-ROR2信号通过RHO依赖性机制在破骨细胞功能中起重要作用。