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Involvement of the Ca(2+) signaling pathway in osteoprotegerin inhibition of osteoclast differentiation and maturation

The purpose of this study was to determine whether the Ca(2+) signaling pathway is involved in the ability of osteoprotegerin (OPG) to inhibit osteoclast differentiation and maturation. RAW264.7 cells were incubated with macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear fa...

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Detalles Bibliográficos
Autores principales: Fu, Yingxiao, Gu, Jianhong, Wang, Yi, Yuan, Yan, Liu, Xuezhong, Bian, Jianchun, Liu, Zong-Ping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Veterinary Science 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4483497/
https://www.ncbi.nlm.nih.gov/pubmed/25549213
http://dx.doi.org/10.4142/jvs.2015.16.2.151
Descripción
Sumario:The purpose of this study was to determine whether the Ca(2+) signaling pathway is involved in the ability of osteoprotegerin (OPG) to inhibit osteoclast differentiation and maturation. RAW264.7 cells were incubated with macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-κB ligand (RANKL) to stimulate osteoclastogenesis and then treated with different concentrations of OPG, an inhibitor of osteoclast differentiation. The intracellular Ca(2+) concentration [Ca(2+)](i) and phosphorylation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in the different treatment groups were measured by flow cytometry and Western blotting, respectively. The results confirmed that M-CSF + RANKL significantly increased [Ca(2+)](i) and CaMKII phosphorylation in osteoclasts (p < 0.01), and that these effects were subsequently decreased by OPG treatment. Exposure to specific inhibitors of the Ca(2+) signaling pathway revealed that these changes varied between the different OPG treatment groups. Findings from the present study indicated that the Ca(2+) signaling pathway is involved in both the regulation of osteoclastogenesis as well as inhibition of osteoclast differentiation and activation by OPG.