miR-296-3p Controls Osteogenic Proliferation and Differentiation by Targeting ICAT and Is Involved in Fracture Healing
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
40627835
DOI
10.14712/fb2025071020064
PII: fb_2025071020064
Knihovny.cz E-resources
- Keywords
- BMSCs, ICAT, fragility fractures, miR-296-3p,
- MeSH
- Cell Differentiation * genetics MeSH
- Fracture Healing * genetics physiology MeSH
- Middle Aged MeSH
- Humans MeSH
- Mesenchymal Stem Cells metabolism cytology MeSH
- MicroRNAs * metabolism genetics MeSH
- Osteogenesis * genetics MeSH
- Cell Proliferation genetics MeSH
- Aged MeSH
- Wnt Signaling Pathway genetics MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- MicroRNAs * MeSH
- MIRN296 microRNA, human MeSH Browser
Fragility fractures have been a cause for concern because of their high incidence. For the prevention and treatment of osteoporotic fractures, it is important to understand how to promote bone formation and increase bone mass. This study investigated miR-296-3p expression and function in fragility fracture. The study enrolled 98 patients with hip fractures, 90 patients with wrist fractures and 35 healthy controls. RT-qPCR was used to detect the miR-296-3p level changes before and after surgery in fracture patients and during the differentiation of human bone mesenchymal stem cells (BMSCs). The starBase bioinformatics database was used for prediction of the miR-296-3p target gene, and dual luciferase report was used for verification of the target relationship. Our results demonstrated that miR-296-3p levels are up-regulated in fracture patients, while they gradually decrease during human BMSC differentiation. The up-regulation of miR-296-3p inhibited the proliferation and differentiation ability of human BMSCs, while inhibition of its expression had the opposite effects. miR-296-3p negatively regulates osteogenic differentiation, and over-expression of inhibitor of β-catenin and TCF (ICAT) could counteract the negative regulatory effect. miR-296-3p targets ICAT and affects the expression of key proteins in the Wnt/β-catenin signalling pathway. In conclusion, miR-296-3p can regulate the division and differentiation of osteoblasts by affecting the expression of ICAT and participate in fracture healing.
Department of Emergency Nantong Haimen District People's Hospital Nantong China
Department of Orthopedic Surgery Affiliated Hospital of Zunyi Medical University Zunyi China
Department of Orthopedics Chonggang General Hospital Chongqing China
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