Vascular endothelial growth factor acts as a survival factor for newly formed retinal vessels and has implications for retinopathy of prematurity

T Alon, I Hemo, A Itin, J Pe'er, J Stone, E Keshet - Nature medicine, 1995 - nature.com
T Alon, I Hemo, A Itin, J Pe'er, J Stone, E Keshet
Nature medicine, 1995nature.com
Retinopathy of prematurity (ROP) is initiated by hyperoxia–induced obliteration of newly
formed blood vessels in the retina of the premature newborn. We propose that vessel
regression is a consequence of hyperoxia–induced withdrawal of a critical vascular survival
factor. We show that regression of retinal capillaries in neonatal rats exposed to high
oxygen, is preceded by a shut–off of vascular endothelial growth factor (VEGF) production
by nearby neuroglial cells. Vessel regression occurs via selective apoptosis of endothelial …
Abstract
Retinopathy of prematurity (ROP) is initiated by hyperoxia–induced obliteration of newly formed blood vessels in the retina of the premature newborn. We propose that vessel regression is a consequence of hyperoxia–induced withdrawal of a critical vascular survival factor. We show that regression of retinal capillaries in neonatal rats exposed to high oxygen, is preceded by a shut–off of vascular endothelial growth factor (VEGF) production by nearby neuroglial cells. Vessel regression occurs via selective apoptosis of endothelial cells. Intraocular injection of VEGF at the onset of experimental hyperoxia prevents apoptotic death of endothelial cells and rescues the retinal vasculature. These findings provide evidence for a specific angiogenic factor acting as a vascular survival factor in vivo. The system also provides a paradigm for vascular remodelling as an adaptive response to an increase in oxygen tension and suggests a novel approach to prevention of ROP.
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