IL1β promotes osteogenic differentiation of mouse bone marrow mesenchymal stem cells via the BMP/Smad pathway within a certain concentration range

Inflammatory factors play an important role in the process of fracture healing. The influence of interleukin (IL)1β, a key inflammatory factory, on new bone formation has been controversial. The aim of the present study was to investigate whether IL1β affects the osteogenic differentiation of mouse bone marrow mesenchymal stem cells (MBMMSCs), and examined its effective concentration range and molecular mechanism of action. MBMMSC proliferation in the presence of IL1β was observed using a CellCounting Kit8 assay, and the effect of IL1β on MBMMSC apoptosis was examined via flow cytometry. Alkaline phosphatase assay, Alizarin Red staining and quantitative assays were performed to evaluate the osteogenic differentiation of MBMMSCs. The expression levels of osteogenic differentiation markers were detected using reverse transcriptionquantitative PCR (RTqPCR). It was demonstrated that within a concentration range of 0.011 ng/ml, IL1β promoted osteogenic differentiation of MBMMSCs and did not induce apoptosis. Furthermore, RTqPCR results indicated that IL1β increased osteogenic gene expression within this concentration range. Moreover, Western blotting results identified that the bone morphogenetic protein/Smad (BMP/Smad) signaling pathway was significantly activated by IL1β under osteogenic conditions. Therefore, the present results suggested that within a certain concentration range, IL1β promoted osteogenic differentiation and function of MBMMSCs via the BMP/Smad signaling pathway.