VEGF and its role in the early development of the long bone epiphysis
Doris Allerstorfer, Stefano Longato, Christoph Schwarzer, Reiner Fischer-Colbrie, Alison R Hayman & Michael J F Blumer
abstract
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In long bones of murine species, undisturbed development of the
epiphysis depends on the generation of vascularized cartilage canals
shortly after birth. Despite its importance, it is still under
discussion how this event is exactly regulated. It was suggested
previously that, following increased hypoxia in the epiphyseal core,
angiogenic factors are expressed and hence stimulate the ingrowth of
the vascularized canals. In the present study, we tested this model
and examined the spatio-temporal distribution of two angiogenic
molecules during early development in mice. In addition, we
investigated the onset of cartilage hypertrophy and mineralization.
Our results provide evidence that the vascular endothelial growth
factor is expressed in the epiphyseal resting cartilage prior to the
moment of canal formation and is continuously expressed until the
establishment of a large secondary ossification centre.
Interestingly, we found no expression of secretoneurin before the
establishment of the canals although this factor attracts blood
vessels under hypoxic conditions. Epiphyseal development further
involves maturation of the resting chondrocytes into hypertrophic
ones, associated with the mineralization of the cartilage matrix and
eventual death of the latter cells. Our results suggest that
vascular endothelial growth factor is the critical molecule for the
generation of the epiphyseal vascular network in mice long bones.
Secretoneurin, however, does not appear to be a player in this
event. Hypertrophic chondrocytes undergo cell death by a mechanism
interpreted as chondroptosis.
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citation
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Allerstorfer D, Longato S, Schwarzer C, Fischer-Colbrie R, Hayman A
R, Blumer M J F. VEGF and its role in the early development of the
long bone epiphysis. J Anat 2010; 216:611-24.
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type
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journal paper/review (English)
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date of publishing
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5-2010
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journal title
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J Anat (216/5)
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ISSN electronic
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1469-7580
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pages
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611-24
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PubMed
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20525089
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DOI
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10.1111/j.1469-7580.2010.01223.x
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