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Gli+ stem cells and the development and repair of craniofacial bones
DOI:10.1038/bonekey.2015.96
It has been previously assumed that craniofacial bones and long bones both have the same injury repair and turnover mechanisms, modulated by perivascular mesenchymal stem cells. In this study, the authors use mouse craniofacial bones as a model and identify Gli1+ cells as the stem cell population responsible for the development of these bones and also their repair after injury.
Gli1 was expressed in the calvarial bones of the mice at birth; initially expression was detected throughout the periosteum, dura and suture mesenchyme but by one month after birth, Gli1 was expressed only in the suture mesenchyme. Gli1+ cells do not show any affinity for vasculature but appear to exist within the osteogenic front in the cranial sutures.
Generation of mice with an incomplete but substantial induced ablation of Gli1+ cells showed that vastly reduced Gli1 expression led to an arrest of skull growth, craniosynostosis, osteoporosis and poor injury repair. The authors also show that Gli1+ cells are present in significantly lower numbers in Twist1+/- mice, an established murine model of synostosis.
Editor's comment: This study demonstrates that Gli1+ cells within the suture mesenchyme are the MSC that support craniofacial bone turnover and injury healing. These cells are distinct from the perivascular MSCs found in the long bones. These results should help our understanding of how craniofacial bone formation is regulated and should tell us more about the pathogenesis of craniofacial disorders.
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