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FRZB affects Staphylococcus aureus‑induced osteomyelitis in human bone marrow derived stem cells by regulating the
Xin Li1, Wenyong Pang1, Hongsong Fan1
1Department of Emergency Surgery, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550023, P.R. China.
Abstract:
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.
Insights
Frizzled related protein (FRZB) exacerbates osteomyelitis by reducing stem cell viability and promoting apoptosis. FRZB activates the Wnt/β-catenin pathway, offering a potential therapeutic target for bone infections.
Area of Science:
- Biomedical Science
- Molecular Biology
- Cell Biology
Background:
- Osteomyelitis is a serious bone infection with significant patient impact.
- Frizzled related protein (FRZB) is implicated in various diseases but its role in osteomyelitis is unknown.
Purpose of the Study:
- To investigate the role and mechanism of FRZB in Staphylococcus aureus-induced osteomyelitis.
- To elucidate FRZB's function in human bone marrow derived stem cells (hBMSCs) under osteomyelitis conditions.
Main Methods:
- hBMSCs were infected with S. aureus in vitro to model osteomyelitis.
- Gene and protein expression analyzed via RT-PCR and Western blotting.
- Cell viability, apoptosis, and differentiation assessed using CCK-8, caspase-3 assay, and Alizarin red staining.
Main Results:
- FRZB expression was upregulated in S. aureus-infected hBMSCs.
- FRZB overexpression decreased cell viability and differentiation, increasing apoptosis.
- FRZB knockdown reversed these effects, and Wnt pathway inhibition partially blocked FRZB downregulation's impact.
Conclusions:
- FRZB plays a regulatory role in osteomyelitis.
- FRZB mediates osteomyelitis by activating the Wnt/β-catenin signaling pathway.
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