[A preliminary study on IL-17A promoting osteoblast differentiation via the Wnt5a/β-catenin pathway]

Objective To investigate the effects of interleukin 17A (IL-17A) on osteoblast differentiation and to further explore whether these effects are mediated via the Wnt5a/β-catenin signaling pathway. Methods MC3T3-E1 pre-osteoblasts and mouse bone mesenchymal stem cells (BMSCs) were treated with IL-17A at concentrations of 0.01, 0.1, 1, and 10 ng/mL. Cell proliferation was measured using the CCK-8 assay. Apoptosis of MC3T3-E1 cells was assessed by flow cytometry, and osteogenic differentiation was evaluated by alkaline phosphatase (ALP) and Alizarin Red S (ARS) staining. Western blotting was performed to determine the expression of phosphorylated nuclear factor κB p65 (p-NF-κB p65), nuclear factor κB subunit (NF-κB p65), nuclear factor κB inhibitor α (IκBα), Wnt5a, β-catenin, and Runt-related transcription factor 2 (Runx2). Results IL-17A promoted MC3T3-E1 cell proliferation in a time- and dose-dependent manner. Compared with the positive control group, the IL-17A group significantly inhibited cell apoptosis. IL-17A enhanced ALP activity and the formation of mineralized nodules in both cell types in a dose-dependent manner. Treatment with IL-17A significantly upregulated the expression levels of p-NF-κB p65, Wnt5a, β-catenin, and Runx2, while markedly downregulating the expression levels of IκBα . Conclusion IL-17A may influence the survival, proliferation, and osteogenic differentiation of osteoprogenitor cells via the Wnt5a/β-catenin signaling pathway.