Thursday, April 24, 2014
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Bone repair; osteoporosis
Hypoxia-inducible factor 1a (HIF1A;
HIF1a); notch 1
Mouse studies suggest
stimulating expansion of a vascular endothelial vessel subtype in bone could
help treat fractures or age-dependent osteoporosis. In mice,
immunohistochemical analysis and lineage tracing showed that a specific type
of branched, proliferative vasculature in a portion of the bone was
associated with osteoprogenitor cells. In aged mice suffering from a loss of
this specific type of vasculature and bone mass, activation of Hif1a transcriptional
activity led to expansion of this vasculature type and increased both
osteoprogenitor cell numbers and bone mass compared with vehicle. In mice,
inactivation of notch signaling in endothelial cells decreased endothelial
cell proliferation and bone formation compared with what was seen in
wild-type controls. In mice with inactivated notch signaling, recombinant noggin
a secreted bone
morphogenetic protein (Bmp)
antagonist induced by Notch1, improved vascularization and formation of bone.
Next steps could include developing targeted approaches for activating HIF1A
or NOTCH1 signaling in bone.
Published online April 24, 2014
Patent and licensing status
Kusumbe, A.P. et al.
Nature; published online March 12, 2014;
Ramasamy, S.K. et al. Nature; published online March 12, 2014;
Contact: Ralf H. Adams, University of Muenster, Muenster,
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