Science Advances

Supplementary Materials

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  • Table S1. Primers used in this study.
  • Fig. S1. CD90+ MSCs were preferentially recruited into fractured bones from progenitor niches near fracture sites.
  • Fig. S2. Soluble factors, secreted by COX-2–transduced cells, augmented the proliferation and CD90+ conversion of CD90 MSCs.
  • Fig. S3. CD90+ mSSCs purified from fractured bones were stable for at least 3 weeks in culture, expressed common MSC markers, and differentiated into osteoblasts in fracture sites.
  • Fig. S4. Effects of COX-2 signaling blockade on the osteogenic potential of CD90+ mSSCs.
  • Fig. S5. COX-2 overexpression in fracture sites augmented local expression of WNT ligands.
  • Fig. S6. Local COX-2 overexpression reduced callus sizes, and this effect was abolished by the administration of the anti-CD90 mAb 30H12 (see Fig. 6 for details of experimental designs).
  • Fig. S7. A model for COX-2 overexpression–mediated acceleration of bone repair.
  • Fig. S8. Delivery of vectors into fracture sites.

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