Analysis of bone and cartilage destruction mechanism via RANKL/Fas signaling in rheumatoid arthritis

2015 Fiscal Year Final Research Report

• Project/Area Number: 25713063
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Partial Multi-year Fund
• Research Field: Orthodontics/Pediatric dentistry
• Research Institution: The University of Tokushima
• Principal Investigator: IZAWA Takashi 徳島大学, 大学院医歯薬学研究部, 助教 (30380017)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 歯学 / 歯科矯正学 / 免疫学 / 病理学 / 細胞・組織 / シグナル伝達 / 関節リウマチ / 破骨細胞

Outline of Final Research Achievements

In this study, we investigated the functions of osteoclasts (OCs) from Fas-mutant MRL/lpr mice, murine model for rheumatoid arthritis (RA). In vitro and in vivo experiments showed hyperfunction of MRL/lpr OCs. Furthermore, the migratory response of MRL/lpr OC precursors to S1P was significantly enhanced. The hyper function of OCs in MRL/lpr mice play a potent role in the pathogenesis for RA with bone and cartilage destruction. Crosstalk between RANK/RANKL signaling and Fas/FasL signaling of OCs may regulate the differentiation and migratory function of OC precursors.

Free Research Field

医歯薬学