Osteoclastogenesis is induced by receptor activator of nuclear factor-κB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF), and can be suppressed by osteoprotegerin (OPG). Beclin1 has a dual role in osteoclastogenesis. However, the role of Beclin1-mediated autophagy during OPG-induced inhibition of osteoclastogenesis remains unclear. Here, we found that Beclin1 and matrix metalloproteinase 9 (MMP-9) expression were increased during osteoclastogenesis. OPG (20, 40, and 80 ng/mL) decreased Src and MMP-9 expression, but augmented Beclin1 expression and fluorescence intensity. Similarly, treatment with the autophagy activator rapamycin increased Beclin1 expression during OPG-induced inhibition of osteoclastogenesis. Further, Beclin1 knockdown restored osteoclast numbers by reducing autophagy during OPG-induced inhibition of osteoclastogenesis. These results indicate that Beclin1 has a positive role during OPG-induced inhibition of osteoclastogenesis by regulating autophagy, which might provide a potential basis for osteoclastogenesis.

破骨细胞生成是由核因子-κB 配体 (RANKL) 和巨噬细胞集落刺激因子 (M-CSF) 的受体激活剂诱导的，并且可以被骨保护素 (OPG) 抑制。Beclin1 在破骨细胞生成中具有双重作用。然而，Beclin1 介导的自噬在 OPG 诱导的破骨细胞生成抑制过程中的作用仍不清楚。在这里，我们发现在破骨细胞生成过程中，Beclin1 和基质金属蛋白酶 9 (MMP-9) 的表达增加。OPG（20、40 和 80 ng/mL）降低了 Src 和 MMP-9 的表达，但增强了 Beclin1 的表达和荧光强度。类似地，在 OPG 诱导的破骨细胞生成抑制过程中，自噬激活剂雷帕霉素治疗增加了 Beclin1 的表达。更远，Beclin1 敲低通过减少 OPG 诱导的破骨细胞生成抑制过程中的自噬来恢复破骨细胞数量。这些结果表明，Beclin1 通过调节自噬在 OPG 诱导的破骨细胞生成抑制中具有积极作用，这可能为破骨细胞生成提供潜在的基础。