BoneKEy Reports | BoneKEy Watch
The role of SDF-1 in fracture repair
DOI:10.1038/bonekey.2012.158
When a traumatic fracture occurs, vascular damage usually leads to tissue hypoxia and altered expression of SDF-1/CXCR4 signaling. This study therefore focused on SDF-1 (also called CXCL12), which previous research has identified as a master regulator of the recruitment of stem cells and progenitor cells to the site of ischemic injury, to investigate its role in fracture healing.
Mice with an induced fracture were injected twice daily with ADM3100, an antagonist of CXCR4, in order to disrupt the recruitment of stem cells to the site of the fracture. The authors then monitored how these fractures healed over 42 days compared to controls.
Treated mice showed a significant reduction in hyaline cartilage at the fracture repair site after 14 days, and a significantly lower callus volume and mineralized bone volume by 45 days. The researchers also noted that expression of genes encoding collagen Type 1 alpha 1, collagen Type 2 alpha 1, vascular endothelial growth factor and other factors involved in endochondral ossification, was reduced.
Editor's comment: Inhibition of SDF-1, which is associated with progenitor cell trafficking, inhibited the chondrogenic stage of fracture healing, suggesting that it is an important regulator of stem cells and progenitor cells. Further research is required to determine whether SDF-1 local agonists could promote fracture repair.
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