Sclerostin deficient mice rapidly heal bone defects by activating β-catenin and increasing intramembranous ossification

Meghan E. McGee-Lawrence, Zachary C. Ryan, Lomeli R. Carpio, Sanjeev Kakar, Jennifer J. Westendorf, Rajiv Kumar

Research output: Contribution to journalArticle

32 Scopus citations

Abstract

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 β-catenin expression than observed in WT mice. The findings were similar to those observed in Axin2-/- mice, in which β-catenin signaling is known to be enhanced to facilitate bone regeneration. Taken together, these data indicate that enhanced β-catenin signaling is present in Sost-/- mice that demonstrate accelerated healing of bone defects, suggesting that modulation of β-catenin signaling in bone could be used to promote fracture repair.

Original languageEnglish (US)
Pages (from-to)886-890
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume441
Issue number4
DOIs
StatePublished - Nov 29 2013

Keywords

  • Fracture healing
  • Intramembranous ossification
  • Osteoblast
  • Sclerostin
  • Wnt
  • β-Catenin

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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