作者: Y.-M. Lee , N. Fujikado , H. Manaka , H. Yasuda , Y. Iwakura
关键词:
摘要: It is well known that IL-1 involved in bone resorption under pathological conditions. The role of this cytokine remodeling physiological conditions, however, remains obscure. In study, we addressed the metabolism through analyses IL-1α-deficient (KO), IL-1β KO and IL-1α/β double mice were housed specific pathogen free femur mineral density, trabecular mass cortical thickness significantly increased all compared with wild-type (WT) mice. number osteoclasts bones decreased, suggesting regulates regulation osteoclast formation. When differentiation marrow (BM) cells into was induced by parathyroid hormone co-cultures osteoblasts BM from WT mice, cell failed to undergo efficient osteoclast-like multinucleated (OCL) differentiation, although high levels receptor activator nuclear factor-κB (NF-κB) ligand (RANKL) induced. contrast, OCL observed osteoblast/WT co-cultures, which low RANKL produced. Addition IL-1α BM-derived macrophage cultures markedly enhanced soluble RANKL, downstream molecules NF-κB (RANK) including c-Jun N-terminal factor, extracellular signal-regulated kinase c-Fos less activated absence upon treatment RANKL. Taken together, these results indicate directly activates RANK signaling other than inducing promote osteoclastogenesis plays an important metabolism.