作者: Juan Xu , Feng Yue , Jingbo Wang , Li Chen , Wenbo Qi
关键词: Biology 、 Osteoclast 、 RANK Ligand 、 Osteoclast fusion 、 Signal transduction 、 Activator (genetics) 、 RANKL 、 Downregulation and upregulation 、 Osteoclast maturation 、 Cell biology 、 Molecular biology
摘要: The balance between bone formation and resorption is compromised in diabetes, which may contribute to the high risk of fractures diabetic patients. However, mechanism by glucose affects turnover remains be elucidated. present study demonstrated that inhibited receptor activator nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis. In order examine involved inhibition osteoclastogenesis, examined several key molecules osteoclast differentiation, including v-ATPase V0 subunit d2 (Atp6V0d2), dendritic cell-specific transmembrane protein (DC-STAMP), c-fos factor activated T cells c1 (NFATc1). expression levels Atp6V0d2 DC-STAMP are regulated NFATc1 c-fos, required for fusion, important maturation. To best our knowledge, first time decreased gene ATP6v0d2 RAW264.7 mediated RANKL. Therefore, suppression pre-osteoclast or fusion essential differentiation.