RANKL 유도성 파골세포 분화에 있어서 LTB4의 역할 규명

Abstract

Leukotriene B4 (LTB4) is a potent lipid mediator of inflammation formed by the 5-lipoxygenase(5-LO)-catalyzed oxidation of arachidonic acid. LTB4 mediates diverse biological activities through two distinct highly conserved G protein-coupled receptors BL T1 and BL T2. In this study, we investigated the role of LTB4 in receptor activator of nuclear factor-kappaB ligand (RANKL)-induced osteoclast formation. 5-lipoxygenase inhibitor and antagonists for BLT1 or BLT2 were shown to suppress the RANKL-induced osteoclast formation in mouse bone marrow-dereived macrophage (BMM) culture system. Furthermore, RT-PCR analysis demonstrated that rnRNA expression levels for 5-LO, BLT1, and BLT2 on BMM cells were significantly increased by the treatment of RANKL. Taken together, these data suggest the possible role of LTB4 on RANKL-induced osteoclast formation.