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MicroRNA-124 inhibits TNF-α- and IL-6-induced osteoclastogenesis

  • Bone and Cartilage
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Abstract

Receptor activator for nuclear factor κB ligand (RANKL)-independent osteoclastogenic pathway was reported recently. MicroRNA (miR)-124 has been known to suppress RANKL-dependent osteoclastogenesis by inhibiting NFATc1 expression. However, whether miR-124 regulates a RANKL-independent pathway has not been elucidated. In this study, we examined whether a RANKL-independent pathway is regulated by miR-124 in addition to the RANKL-dependent one. Using osteoclastogenic culture and pit-formation assay, we found that a miR-124 mimic inhibited osteoclastogenesis in mouse bone marrow-derived macrophages stimulated by TNF-α, IL-6, and M-CSF in the presence of osteoprotegerin. We also showed that the expression levels of osteoclast-specific genes and NFATc1 protein were suppressed in the miR-124 mimic-transfected cells by performing quantitative-polymerase chain reaction and western blotting. Our results indicate that miR-124 is important in inhibiting both RANKL-dependent and -independent osteoclast differentiation by suppressing NFATc1-mediated pathway.

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Acknowledgements

We would like to thank Clarity Editing for English proofreading.

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Authors and Affiliations

Authors

Contributions

Conceptualization: SK. Data curation and making figures and graphs: KO. Formal analysis: SK, JS. Investigation: YN, YN, KU. Methodology: SK, JS, SK. Integration of the study: KO, SK, JS, SK. Supervision: SK. Writing ± original draft: KO. Writing ± review and editing: SK, JS, SK.

Corresponding author

Correspondence to Seiji Kawano.

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Conflict of interest

The authors declare no conflicts of interest. This study was approved by the Institutional Animal Care and Use Committee of Kobe University.

Additional information

We reported the data included in this manuscript in the 65th Annual Meeting of Japanese Society of Laboratory Medicine.

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Ohnuma, K., Kasagi, S., Uto, K. et al. MicroRNA-124 inhibits TNF-α- and IL-6-induced osteoclastogenesis. Rheumatol Int 39, 689–695 (2019). https://doi.org/10.1007/s00296-018-4218-7

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  • DOI: https://doi.org/10.1007/s00296-018-4218-7

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