TNFRSF11B-modified umbilical cord mesenchymal stem cells as a novel strategy for bone-related diseases by suppressing osteoclast activity
Ding M., Ding Q., Liu Z., Wang L., Pei K., Hu J.
Laboratory Study, published in J Orthop Surg Res (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- J Orthop Surg Res (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 40380204
- PMCID
- PMC12085028
- DOI
- 10.1186/s13018-025-05850-9
- Citations
- 2
Abstract (original English)
Background and objective Mesenchymal stem cells (MSCs), possessing multilineage potential, are capable of differentiating into osteoblasts and thus serve as suitable seed cells for bone regeneration. Tumor necrosis factor receptor superfamily member 11B (TNFRSF11B) gene encodes osteoprotegerin (OPG), which has a critical role in repressing osteoclast differentiation and has been reported to influence the adipogenic differentiation of bone marrow mesenchymal stem cells (BMMSCs). Nevertheless, the impact of TNFRSF11B on the osteogenic differentiation of umbilical cord mesenchymal stem cells (UCMSCs) remains unclear. This study aimed to investigate the role of TNFRSF11B in the osteogenesis of UCMSCs and bone remodeling. Methods Differentially expressed genes (DEGs) were identified from the GEO database using R software. TNFRSF11B was transduced into UCMSCs by a lentiviral vector. Cell differentiation capacity was assessed by ALP staining, TRAP staining, and qRT-PCR assay. Proteomic analysis was performed to investigate the key proteins in TNFRSF11B-OE-UCMSCs that inhibit osteoclast differentiation. Results We found that the TNFRSF11B gene was upregulated during osteogenic differentiation and downregulated during adipogenic differentiation of UCMSCs. UCMSCs overexpressing the TNFRSF11B gene were successfully generated via lentivirus transfection. However, neither the overexpression
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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