Oncostatin M promotes the osteogenic differentiation of mouse MC3T3‑E1osteoblasts through the regulation of monocyte chemotactic protein‑1.

The present study investigated the function of oncostatin M (OSM), which may be associated with monocyte chemotactic protein‑1 (MCP‑1), on mouse MC3T3‑E1 osteoblast development and bone remodeling. Levels of MCP‑1, macrophage inflammatory protein 1α (MIP1α) and regulated upon activation normal T cell expressed and secreted (RANTES) were measured by ELISA. Cell viability, migration and invasion abilities were detected by MTT, wound healing and Transwell assays, respectively. Western blotting was performed to detect levels of phosphorylated protein kinase B (Akt). Reverse transcription‑quantitative polymerase chain reaction and western blotting were performed to detect the levels of matrix metalloproteinases (MMP)‑1, ‑2 and ‑3. The results demonstrated that OSM treatment significantly increased MCP‑1 levels in a dose‑dependent manner. Interleukin (IL)‑1, also significantly increased MCP‑1 levels; however, treatment with other cytokines, including IL‑6, IL‑11 and leukemia inhibitory factor did not affect MCP‑1 levels to the same extent. In addition, OSM did not affect levels of the chemokines MIP1α and RANTES; indeed, only IL‑1 significantly increased levels of MIP1α and RANTES. OSM treatment promoted the proliferation, migration and invasion in a dose‑dependent manner, which were inhibited by MCP‑1 silencing. The expression of phosphorylated‑Akt, MMP‑1, ‑2 and ‑3 were increased by OSM treatment; however, these increases were reversed following MCP‑1 silencing. Collectively these data suggest that OSM promotes the differentiation of mouse MC3T3‑E1 osteoblasts via regulation of MCP‑1 expression. These results may therefore provide novel insights into bone repair and remodeling.