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Lack of ADAM10 in endothelial cells affects osteoclasts at the chondro-osseus junction.
- Source :
-
Journal of Orthopaedic Research . Feb2014, Vol. 32 Issue 2, p224-230. 7p. - Publication Year :
- 2014
-
Abstract
- Mice lacking ADAM10 in endothelial cells ( Adam10ΔEC mice) have shorter femurs, tibiae, and humeri than controls, raising questions about how endothelial cells could control long bone growth. We performed a histopathological evaluation of the femur and tibia growth plates at different postnatal stages, and assessed the distribution of TRAP-positive osteoclasts and endothelial cells at the growth plate. The growth plates in Adam10ΔEC mice appeared normal at P7 and P14, but a thickened zone of hypertrophic chondrocytes and increased trabecular bone density were apparent by P21 and later. The number of TRAP+ cells at the COJ was normal at P7 and P14, but was strongly reduced at P21 and later. Moreover, the density of endomucin-stained endothelial cells at the COJ was increased starting at P7. The defects in long bone growth in Adam10ΔEC mice could be caused by a lack of osteoclastogenesis at the COJ. Moreover, ADAM10 appears to regulate endothelial cell organization in the developing bone vasculature, perhaps in a similar manner as in the developing retinal vascular tree, where ADAM10 is thought to control Notch-dependent endothelial cell fate decisions. This study provides evidence for the regulation of osteoclast function by endothelial cells in vivo. © 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:224-230, 2014. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 07360266
- Volume :
- 32
- Issue :
- 2
- Database :
- Academic Search Index
- Journal :
- Journal of Orthopaedic Research
- Publication Type :
- Academic Journal
- Accession number :
- 92983748
- Full Text :
- https://doi.org/10.1002/jor.22492