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Tissue Eng Part A. 2011 Aug;17(15-16):2061-9. doi: 10.1089/ten.TEA.2010.0719. Epub 2011 Jun 1.

Fgf-18 is required for osteogenesis but not angiogenesis during long bone repair.

Author information

1
Hagey Laboratory, Department of Surgery, Stanford University School of Medicine, Stanford, California 94305, USA.

Abstract

Bone regeneration is a complex event that requires the interaction of numerous growth factors. Fibroblast growth factor (Fgf)-ligands have been previously described for their importance in osteogenesis during development. In the current study, we investigated the role of Fgf-18 during bone regeneration. By utilizing a unicortical tibial defect model, we revealed that mice haploinsufficient for Fgf-18 have a markedly reduced healing capacity as compared with wild-type mice. Reduced levels of Runx2 and Osteocalcin but not Vegfa accompanied the impaired bone regeneration. Interestingly, our data indicated that upon injury angiogenesis was not impaired in Fgf-18(+/-) mice. Moreover, other Fgf-ligands and Bmp-2 could not compensate for the loss of Fgf-18. Finally, application of FGF-18 protein was able to rescue the impaired healing in Fgf-18(+/-) mice. Thus, we identified Fgf-18 as an important mediator of bone regeneration, which is required during later stages of bone regeneration. This study provides hints on how to engineering efficiently programmed bony tissue for long bone repair.

PMID:
21457097
PMCID:
PMC3142654
DOI:
10.1089/ten.TEA.2010.0719
[Indexed for MEDLINE]
Free PMC Article
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