FRZB affects Staphylococcus aureus‑induced osteomyelitis in human bone marrow derived stem cells by regulating the Wnt/β‑catenin signaling pathway.

Osteomyelitis is an infectious disease of bone tissue caused by bacterial infection, which can infect through hematogenous, traumatic or secondary ways and then lead to acute or chronic bone injury and relative clinical symptoms, bringing physical injury and economic burden to patients. Frizzled related protein (FRZB) participates in the regulation of various diseases (osteoarthritis, cardiovascular diseases and types of cancer) by regulating cell proliferation, motility, differentiation and inflammation, while its function in osteomyelitis remains to be elucidated. The present study aimed to uncover the role and underlying mechanism of FRZB mediation in Staphylococcus aureus (S. aureus)-induced osteomyelitis. Human bone marrow derived stem cells (hBMSCs) were treated with S. aureus to imitate an inflammatory osteomyelitis micro-environment in vitro, then mRNA and protein expression were severally assessed by RT-PCR and western blotting. The activity, apoptosis and differentiation of the cells were characterized via CCK-8, caspase-3 activity and Alizarin red sulfate/alkaline phosphatase staining, respectively. Expression levels of FRZB were upregulated in S. aureus-infected hBMSCs. Over-expression of FRZB significantly reduced hBMSC cell viability and differentiation while promoting cell apoptosis with or without S. aureus infection. However, FRZB knockdown reversed these effects. Once Wnt was impeded, the effect of FRZB downregulation was impeded to a great extent. Taken together, FRZB participated to regulate the osteomyelitis by activating the Wnt/β-catenin signaling pathway.