| First Author | McGee-Lawrence ME | Year | 2013 |
| Journal | Biochem Biophys Res Commun | Volume | 441 |
| Issue | 4 | Pages | 886-90 |
| PubMed ID | 24211207 | Mgi Jnum | J:211503 |
| Mgi Id | MGI:5575593 | Doi | 10.1016/j.bbrc.2013.10.155 |
| Citation | McGee-Lawrence ME, et al. (2013) Sclerostin deficient mice rapidly heal bone defects by activating beta-catenin and increasing intramembranous ossification. Biochem Biophys Res Commun 441(4):886-90 |
| abstractText | We investigated the influence of the osteocyte protein, sclerostin, on fracture healing by examining the dynamics and mechanisms of repair of single-cortex, stabilized femoral defects in sclerostin knockout (Sost(-/-); KO) and sclerostin wild-type (Sost(+/+); WT) mice. Fourteen days following generation of bone defects, Sost KO mice had significantly more bone in the healing defect than WT mice. The increase in regenerating bone was due to an increase in the thickness of trabecularized spicules, osteoblast numbers and surfaces within the defect. Enhanced healing of bone defects in Sost KO mice was associated with significantly more activated beta-catenin expression than observed in WT mice. The findings were similar to those observed in Axin2(-/-) mice, in which beta-catenin signaling is known to be enhanced to facilitate bone regeneration. Taken together, these data indicate that enhanced beta-catenin signaling is present in Sost(-/-) mice that demonstrate accelerated healing of bone defects, suggesting that modulation of beta-catenin signaling in bone could be used to promote fracture repair. |
