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Department of Molecular Biology, The Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel
Development of
microvascular networks is set to meet the metabolic requirements of the
tissue they perfuse. Accordingly, impairment of oxygen homeostasis,
either due to increased oxygen consumption or as a result of blood
vessel occlusion, triggers compensatory neovascularization. This
feedback reaction is mediated by a hypoxia- and hypoglycemia-induced
vascular endothelial growth factor (VEGF). VEGF accumulates under
stress as a result of increased hypoxia-inducible factor-1
-mediated
transcription, stabilization of the mRNA, and the function of a
hypoxia-refractory internal ribosome entry site within its
5'-untranslated region. Matching of vascular density to the metabolic
needs of the tissue may include a process of hyperoxia-induced vessel
regression. Thus newly formed vascular networks may undergo a natural
process of vascular pruning that takes place whenever VEGF, acting as a
vascular survival factor, is downregulated below the level required to
sustain immature vessels. Immature vessels are particularly vulnerable
and are selectively obliterated upon withdrawal of VEGF. The plasticity window for vessel regression is determined by a delay in the
recruitment of periendothelial cells to the preformed endothelial
plexus. Thus fine-tuning of microvascular density takes place mostly in the newly formed plexus, but the mature system is refractory to episodic changes in tissue oxygenation. These regulatory links may
malfunction in certain pathological settings.
angiogenesis; hypoxia; hyperoxia; vessel regression
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