CXCR4 Antagonism to Treat Delayed Fracture Healing

  title={CXCR4 Antagonism to Treat Delayed Fracture Healing},
  author={Richard L. Meeson and Anita Sanghani-Keri and Melanie J. Coathup and Gordon W Blunn},
  journal={Tissue Engineering. Part A},
  pages={1242 - 1250}
A significant number of fractures develop nonunion. Stem cell homing is regulated through stromal cell-derived factor 1 (SDF1) and its receptor CXCR4. Stem/progenitor cell populations can be endogenously mobilized by administering growth factors with a pharmacological antagonist of CXCR4, AMD3100, which may be a means to improve fracture healing. A 1.5 mm femoral osteotomy in Wistar rats was stabilized with an external fixator. Rats were pretreated with phosphate buffered saline [PBS(P… 
4 Citations

Figures and Tables from this paper

The role of intermittent PTH administration in conjunction with allogenic stem cell treatment to stimulate fracture healing

The beneficial effect of localized MSC injections on fracture healing combined with low- or high-dose teriparatide, with efficacy dependent on PTH dose is demonstrated.

Cerium oxide nanoparticles protect against irradiation-induced cellular damage while augmenting osteogenesis.



Long‐term administration of AMD3100, an antagonist of SDF‐1/CXCR4 signaling, alters fracture repair

The data suggest that the SDF‐1/CXCR4 signaling plays a central role in bone healing possibly by regulating the recruitment and/or differentiation of stem and progenitor cells.

Effect of SDF-1/Cxcr4 Signaling Antagonist AMD3100 on Bone Mineralization in Distraction Osteogenesis

It is demonstrated that the DO process induced higher expression of SDF-1, which collated to rapid induction of callus formation, which may represent a potential therapeutic approach to the enhancement of bone consolidation in patients undergoing DO.

Five Days Granulocyte Colony-Stimulating Factor Treatment Increases Bone Formation and Reduces Gap Size of a Rat Segmental Bone Defect: A Pilot Study

It is hypothesized, that treatment with granulocyte colony-stimulating factor (G-CSF) may improve bone healing by mobilization of CD34+ progenitor cells into the circulation, which in turn may facilitate vascularization at the defect site.

Progenitor Cell Mobilization Enhances Bone Healing by Means of Improved Neovascularization and Osteogenesis

Improved bone regeneration in this model was associated with elevated circulating progenitor cell number and subsequently improved neovascularization and osteogenesis, highlighting the importance of circulating progentitor cells in bone healing and may provide a novel therapy for bone regeneration.

Clinical impact of circulating CD34-positive cells on bone regeneration and healing.

The first proof-of-principle experiments demonstrating the collaborative characteristics of circulating CD34(+) cells, known as endothelial and hematopoietic progenitor cell-rich population, which are capable to differentiate into both endothelial cells and osteoblasts are performed.

Circulating cells with osteogenic potential are physiologically mobilized into the fracture healing site in the parabiotic mice model

Data indicate that circulating osteogenic CTPs are mobilized to fracture site and contribute to osteogenesis in the early stage of fracture healing.

VEGF-activated angiogenesis during bone regeneration.

Significance of circulating endothelial progenitor cells in patients with fracture healing process

Findings suggest traumatic fracture may induce the mobilization of EPCs into the peripheral circulation, and the increased E PCs may contribute to neovascularization and involve in fracture healing.