Journal article
Loss of ephrinB1 in osteogenic progenitor cells impedes endochondral ossification and compromises bone strength integrity during skeletal development
TM Nguyen, A Arthur, S Paton, S Hemming, R Panagopoulos, J Codrington, CR Walkley, ACW Zannettino, S Gronthos
Bone | ELSEVIER SCIENCE INC | Published : 2016
Abstract
The EphB receptor tyrosine kinase family and their ephrinB ligands have been implicated as mediators of skeletal development and bone homeostasis in humans, where mutations in ephrinB1 contribute to frontonasal dysplasia and coronal craniosynostosis. In mouse models, ephrinB1 has been shown to be a critical factor mediating osteoblast function. The present study examined the functional importance of ephrinB1 during endochondral ossification using the Cre recombination system with targeted deletion of ephrinB1 (EfnB1fl/fl) in osteogenic progenitor cells, under the control of the osterix (Osx:Cre) promoter. The Osx:EfnB1−/− mice displayed aberrant bone growth during embryonic and postnatal ske..
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Awarded by National Health and Medical Research Council
Funding Acknowledgements
This work was supported by NHMRC project grant APP1083804, fellowship APP1042677 and the Mary Overton Research Fellowship. We would like to thank Dr. Stephen Fitter, Dr. Sally Martin for establishing and assistance with the Osx:Cre colony and Ms. Nichola Smith for maintaining all the colonies. We appreciate the technical support with Micro-CT imaging and analysis provided by the University Adelaide Microscopy Service. We value the use of laboratory equipment provided by A/Prof. David Haynes at the University of Adelaide and Dr. Julia Kuliwaba at SA Pathology.