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

Abstract

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.

3D printed Ti-5Cu alloy accelerates osteogenic differentiation of MC3T3-E1 cells by stimulating the M2 phenotype polarization of macrophages

“…Several scholars have studied the osteogenic differentiation mechanism of OSM on MC3T3-E1 cells. Zheng et al (59) revealed that OSM promoted the osteogenic differentiation of MC3T3-E1 through MMP-1. It has also been found that Notch signaling pathway plays a negative regulatory role in OSM promoting MC3T3-E1 osteogenic differentiation (24).…”

Intersection between macrophages and periodontal pathogens in periodontitis

“…36 Besides, oncostatin M (OSM) is a member of IL-6 family and induces matrix metalloproteinases (MMPs) expression in a variety of animal cells. [37][38][39] Increased OSM was found in gingival crevicular fluid in periodontitis patients. Simultaneously, exposed to T. d in vitro increased the synthesis and release of OSM in Mϕs.…”

“…In addition, P. g might control the plasticity of Mϕs by preventing the Mϕs from transforming into the M2 subtype in the tissue and redirecting M2 cells to be polarized to the pro‐inflammatory M1 subtype, leading to an over‐inflammatory environment, impairing Mϕs’ ability to repair damaged periodontal tissues 36 . Besides, oncostatin M (OSM) is a member of IL‐6 family and induces matrix metalloproteinases (MMPs) expression in a variety of animal cells 37–39 . Increased OSM was found in gingival crevicular fluid in periodontitis patients.…”

Multifaceted oncostatin M: novel roles and therapeutic potential of the oncostatin M signaling in rheumatoid arthritis

“…OSM also has the ability to promote the proliferation and osteogenic differentiation of osteoblasts. OSM can promote osteogenic differentiation of mouse embryo osteoblast precursor cells MC3T3-E1 by regulating CCL2 (74). Additionally, OSM can promote osteoclast differentiation.…”