Open Access

Temporal differential effects of proinflammatory cytokines on osteoclastogenesis

  • Authors:
    • Su-Jin Moon
    • Inhye E. Ahn
    • Hyerin Jung
    • Hyoju Yi
    • Juryun Kim
    • Youngkyun Kim
    • Seung‑Ki  Kwok
    • Kyung-Su Park
    • Jun‑Ki  Min
    • Sung-Hwan Park
    • Ho-Youn Kim
    • Ji Hyeon Ju
  • View Affiliations

  • Published online on: February 5, 2013     https://doi.org/10.3892/ijmm.2013.1269
  • Pages: 769-777
  • Copyright: © Moon et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

Bone destruction and inflammation are closely linked. Cytokines play an important role in inflammatory bone destruction by upregulating the receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL). The direct role of cytokines that act in a non-RANKL-dependent manner has yet to be elucidated. The aim of this study was to investigate the direct osteoclastogenic properties of inflammatory cytokines at different time-points of osteoclastogenesis. Mouse bone marrow macrophages were stimulated with the macrophage colony-stimulating factor (M-CSF) and various concentrations of RANKL. Inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-17 and IL-23, were added to the culture system of osteoclastogenesis. Two time-points of cytokine treatment were set. The ‘early’ effect of each cytokine was investigated at the time of first RANKL treatment, whereas the ‘late’ effect was investigated 48 h after the first RANKL challenge. Osteoclast differentiation and function were assessed using an osteoclast marker [tartrate-resistant acid phosphatase (TRAP)] and by visualization of pit formation. A permissive level of RANKL was required for cytokine-associated osteoclastogenesis in all experiments. In the M-CSF/RANKL monocellular culture system, IL-1β enhanced and IL-6 decreased osteoclast formation in a dose-dependent manner, regardless of temporal differences. Other cytokines showed various responses according to the phase of osteoclast maturation and the concentration of each cytokine and RANKL. Furthermore, luciferase assays showed that both IL-1β and RANKL activated the NF-κB signaling pathway. Collectively, our data revealed that targeting IL-1β may be a promising strategy to inhibit inflammation-associated bone destruction and osteoporosis.
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April 2013
Volume 31 Issue 4

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Moon S, Ahn IE, Jung H, Yi H, Kim J, Kim Y, Kwok SK, Park K, Min JK, Park S, Park S, et al: Temporal differential effects of proinflammatory cytokines on osteoclastogenesis. Int J Mol Med 31: 769-777, 2013
APA
Moon, S., Ahn, I.E., Jung, H., Yi, H., Kim, J., Kim, Y. ... Ju, J.H. (2013). Temporal differential effects of proinflammatory cytokines on osteoclastogenesis. International Journal of Molecular Medicine, 31, 769-777. https://doi.org/10.3892/ijmm.2013.1269
MLA
Moon, S., Ahn, I. E., Jung, H., Yi, H., Kim, J., Kim, Y., Kwok, S., Park, K., Min, J., Park, S., Kim, H., Ju, J. H."Temporal differential effects of proinflammatory cytokines on osteoclastogenesis". International Journal of Molecular Medicine 31.4 (2013): 769-777.
Chicago
Moon, S., Ahn, I. E., Jung, H., Yi, H., Kim, J., Kim, Y., Kwok, S., Park, K., Min, J., Park, S., Kim, H., Ju, J. H."Temporal differential effects of proinflammatory cytokines on osteoclastogenesis". International Journal of Molecular Medicine 31, no. 4 (2013): 769-777. https://doi.org/10.3892/ijmm.2013.1269