VASCULAR ENDOTHELIAL GROWTH-FACTOR ACTS AS A SURVIVAL FACTOR FOR NEWLY FORMED RETINAL-VESSELS AND HAS IMPLICATIONS FOR RETINOPATHY OF PREMATURITY
VASCULAR ENDOTHELIAL GROWTH-FACTOR ACTS AS A SURVIVAL FACTOR FOR NEWLY FORMED RETINAL-VESSELS AND HAS IMPLICATIONS FOR RETINOPATHY OF PREMATURITY
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DOI：
10.1038/nm1095-1024
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发表时间：
1995-10-01
期刊：
影响因子：
82.9
通讯作者：
KESHET, E
中科院分区：
文献类型：
--
作者：
ALON, T;HEMO, I;KESHET, E
早产儿视网膜病变（ROP）是由早产新生儿视网膜中新形成的血管的高氧诱导闭塞引起的。我们认为，血管退化是高氧诱导的一个关键血管存活因子撤退的结果。我们发现，在新生大鼠暴露于高氧视网膜毛细血管的回归，之前关闭的血管内皮生长因子（VEGF）的生产附近的神经胶质细胞。血管退化通过内皮细胞的选择性凋亡发生。在实验性高氧发作时眼内注射VEGF可防止内皮细胞凋亡并挽救视网膜血管。这些发现为一种特异性血管生成因子在体内作为血管存活因子提供了证据。该系统还提供了一个范例，血管重塑作为一种适应性反应，增加氧张力，并提出了一种新的方法来预防ROP。
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.