Elucidation of mechanisms underlying inflammation-induced LOX-1-dependent RANKL expression in osteoblasts

2015 Fiscal Year Final Research Report

• Project/Area Number: 26870540
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Morphological basic dentistry; Pathobiological dentistry/Dental radiology
• Research Institution: Meikai University
• Principal Investigator: Ito Junta 明海大学, 歯学部, 助教 (40609096)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: LOX-1 / 炎症性骨破壊 / 破骨細胞 / 骨芽細胞 / RANKL

Outline of Final Research Achievements

This study was aimed to clarify the relationship between osteoblastic RANKL expression and lectin-like oxidized LDL receptor-1 (LOX-1) in inflammatory bone destruction. I found that the RANKL expression in the inflamed bones was dependent on LOX-1 that was expressed in osteoblasts. In the co-culture of LOX-1-deleted osteoblasts and wild-type osteoclast precursors, the osteoclastogenesis induced by interleukin-1b and prostaglandin E2 decreased; this process occurred in parallel with the downregulation of osteoblastic RANKL expression. These results indicate that LOX-1-dependent osteoblastic RANKL expression in response to inflammation in bones promote osteoclast formation and bone resorption, suggesting that the blockage of LOX-1 could be a therapeutic target for inflammatory bone disease.

Free Research Field

医歯薬学