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SDF-1/CXCR4 axis acclerates fracture healing after brain injury
DOI:10.1038/bonekey.2013.52
Liu et al. used a mouse model to determine the impact of traumatic brain injury (TBI) on fracture healing.
All mice with an induced femoral fracture showed higher levels of stromal cell-derived factor-1 (SDF-1) at the endosteum and growth plate at the fracture site. Compared with mice with a femoral fracture only, mice with a TBI and femoral fracture showed enhanced callus formation and had 3.5 times higher levels of SDF-1 mRNA in the tissue surrounding the fracture at day 1 (P<0.001). Levels of CXCR4 mRNA (the receptor for SDF-1) were 4.8 times higher (P<0.001).
Inhibition of SDF-1 using a neutralizing antibody reduced callus formation in the TBI/femoral fracture mice. Further experiments in vitro and in vivo confirmed that SDF-1 acts as a chemoattractant for mesenchymal stem cells (MSCs) during the process of endochondral bone repair.
Editor’s comment: Several recent studies have focused on the SDF-1/CXCR4 axis and its role in promoting the ‘homing in’ of MSCs during bone repair. This study shows upregulation of the SDF-1/CXCR4 axis in the context of a traumatic brain injury. Activation of the SDF-1/CXCR4 axis could explain the acceleration in callus formation seen in TBI/femoral fracture mice and the observation that patients with a TBI show enhanced healing reactions and heterotopic ossification.
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