Melatonin inhibits RANKL‑induced osteoclastogenesis through the miR‑882/Rev‑erbα axis in Raw264.7 cells
- Yihao Tian
- Zunlei Gong
- Rui Zhao
- Yue Zhu
Affiliations: Department of Orthopaedics, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China
- Published online on: December 16, 2020 https://doi.org/10.3892/ijmm.2020.4820
Copyright: © Tian
et al. This is an open access article distributed under the
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Melatonin, secreted in a typical diurnal rhythm pattern, has been reported to prevent osteoporosis; however, its role in osteoclastogenesis remains unclear. In the present study, the ability of melatonin to inhibit receptor activator of nuclear factor‑κB ligand (RANKL)‑induced osteoclastogenesis and the associated mechanism were investigated. Raw264.7 cells were cultured with RANKL (100 ng/ml) and macrophage colony‑stimulating factor (M‑CSF; 30 ng/ml) for 7 days, and tartrate‑resistant acid phosphatase (TRAP) staining was used to detect osteoclastogenesis following treatment with melatonin. In addition, the effect of melatonin on cathepsin K and microRNA (miR)‑882 expression was investigated via western blotting and reverse transcription‑quantitative PCR. Melatonin significantly inhibited RANKL‑induced osteoclastogenesis in Raw264.7 cells. From bioinformatics analysis, it was inferred that nuclear receptor subfamily 1 group D member 1 (NR1D1/Rev‑erbα) may be a target of miR‑882. In vitro, melatonin upregulated Rev‑erbα expression and downregulated miR‑882 expression in the osteoclastogenesis model. Rev‑erbα overexpression boosted the anti‑osteoclastogenesis effects of melatonin, whereas miR‑882 partially diminished these effects. The present results indicated that the miR‑882/Rev‑erbα axis may serve a vital role in inhibiting osteoclastogenesis following RANKL and M‑CSF treatment, indicating that Rev‑erbα agonism or miR‑882 inhibition may represent mechanisms through which melatonin prevents osteoporosis.