Alon T, Hemo I, Itin A, Pe'er J, Stone J, Keshet E
Department of Molecular Biology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Nat Med. 1995 Oct;1(10):1024-8. doi: 10.1038/nm1095-1024.
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.
早产儿视网膜病变（ROP）是由高氧诱导早产新生儿视网膜中新形成血管闭塞引发的。我们提出血管消退是高氧诱导关键血管存活因子缺失的结果。我们发现，暴露于高氧环境下的新生大鼠视网膜毛细血管消退之前，附近神经胶质细胞会停止产生血管内皮生长因子（VEGF）。血管消退通过内皮细胞的选择性凋亡发生。在实验性高氧开始时眼内注射VEGF可防止内皮细胞凋亡死亡并挽救视网膜血管系统。这些发现为一种在体内作为血管存活因子的特定血管生成因子提供了证据。该系统还为作为对氧张力增加的适应性反应的血管重塑提供了范例，并提示了一种预防ROP的新方法。
