CD97 inhibits osteoclast differentiation via Rap1a/ERK pathway under compression  

作　　者：Xuan Zhou Xinjia Cai Fengyang Jing Xuefen Li Jianyun Zhang Heyu Zhang Tiejun Li 

机构地区：[1]Department of Oral Pathology,Peking University School and Hospital of Stomatology&National Center of Stomatology&National Clinical Research Center for Oral Diseases&National Engineering Laboratory for Digital and Material Technology of Stomatology&Beijing Key Laboratory of Digital Stomatology&Research Center of Engineering and Technology for Computerized Dentistry Ministry of Health&NMPA Key Laboratory for Dental Materials,Beijing,China [2]Research Unit of Precision Pathologic Diagnosis in Tumors of the Oral and Maxillofacial Regions,Chinese Academy of Medical Sciences(2019RU034),Beijing,China [3]Central Laboratory,Peking University School and Hospital of Stomatology,Beijing,China

出　　处：《International Journal of Oral Science》2024年第1期134-144,共11页国际口腔科学杂志（英文版）

基　　金：supported by the Natural Science Foundation of Hebei Province (H2020206226);Hebei Province Science and Technology Support Program (18277756D);the Science and Technology Research Project of Hebei Higher Education Institutions (ZD2022010);High-level Talent Funding Project of Hebei (C20231141) to W.W。

摘　　要：Acceleration of tooth movement during orthodontic treatment is challenging, with osteoclast-mediated bone resorption on the compressive side being the rate-limiting step. Recent studies have demonstrated that mechanoreceptors on the surface of monocytes/macrophages, especially adhesion G protein-coupled receptors (aGPCRs), play important roles in force sensing.However, its role in the regulation of osteoclast differentiation remains unclear. Herein, through single-cell analysis, we revealed that CD97, a novel mechanosensitive aGPCR, was expressed in macrophages. Compression upregulated CD97 expression and inhibited osteoclast differentiation;while knockdown of CD97 partially rescued osteoclast differentiation. It suggests that CD97 may be an important mechanosensitive receptor during osteoclast differentiation. RNA sequencing analysis showed that the Rap1a/ERK signalling pathway mediates the effects of CD97 on osteoclast differentiation under compression. Consistently, we clarified that administration of the Rap1a inhibitor GGTI298 increased osteoclast activity, thereby accelerating tooth movement. In conclusion,our results indicate that CD97 suppresses osteoclast differentiation through the Rap1a/ERK signalling pathway under orthodontic compressive force.

关 键 词：CD97 OSTEOCLAST inhibited 

分 类 号：R783.5[医药卫生—口腔医学]