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Accelerating Bone Fracture Healing: A Novel Strategy Investigating the Regulation of Mitochondrial Dynamics by BMP-5 Overexpression in Mesenchymal Stem Cells
Vol 38, Issue 4, 2024
Abstract
Background: Bone fracture is a common injury, and the healing process involves the intricate regulation of multiple cells and signaling pathways. Bone Morphogenetic Protein-5 (BMP-5) plays a crucial role as a bone morphogenetic protein in the healing of bone fractures. This study aims to investigate the precise mechanism of BMP-5 in fracture healing. Methods: Mouse mesenchymal stem cells (MSCs) were used as the research model to explore the role of BMP-5 in bone fracture healing. Models of MSCs with BMP-5 knockdown and BMP-5 overexpression were established. The study investigated the effects of BMP-5 on the osteogenic differentiation ability of MSCs, the activity of the β-catenin and Extracellular Signal-Regulated Kinase (ERK) 1/2 signaling pathways, as well as mitochondrial dynamics using quantitative real-time polymerase chain reaction (qRT-PCR), Western blot, and immunofluorescence staining. Additionally, the impact of BMP-5 on fracture-healing tissues was assessed through histological analysis and tube formation assays. Results: The experimental results demonstrated that silencing BMP-5 expression significantly hindered the osteogenic differentiation potential of murine peripheral blood-derived MSCs (mPB-MSCs) (p < 0.05). Conversely, the overexpression of BMP-5 substantially enhanced the osteogenic differentiation ability of mPB-MSCs (p < 0.05). Additionally, BMP-5 overexpression elevated the activity of the β-catenin and ERK1/2 signaling pathways in mPB-MSCs and modulated mitochondrial dynamics (p < 0.05). Histological analysis and tube formation assay results revealed that BMP-5 overexpression in mPB-MSCs promoted angiogenesis and enhanced tube formation capacity in the tissue during bone fracture healing. Conclusions: The upregulation of BMP-5 can promote the osteogenic differentiation of mPB-MSCs and angiogenesis in fracture healing by activating the Wnt/β-catenin and ERK1/2 signaling pathways and enhancing mitochondrial dynamics.
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Copyright (c) 2024 Shaoxian Liu, Jingjie Luan
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Medical Genetics, University of Torino Medical School, Italy
Department of Biomedical, Surgical and Dental Sciences, University of Milan, Italy