Spyridopoulos I, Brogi E, Kearney M, Sullivan A B, Cetrulo C, Isner J M, Losordo D W
St Elizabeth's Medical Center, Department of Medicine, Boston, MA 02134, USA.
J Mol Cell Cardiol. 1997 May;29(5):1321-30. doi: 10.1006/jmcc.1996.0365.
A series of experiments was performed to determine whether vascular endothelial growth factor (VEGF), in addition to its endothelial cell specific mitogenic activity, can also protect endothelial cells from toxin-induced programmed cell death. Apoptosis was induced in endothelial cell culture with tumor necrosis factor-alpha (TNF-alpha). Simultaneous exposure of endothelial cells to VEGF resulted in a dose dependent inhibition of apoptosis when evaluated by: (1) direct counting of cells with morphologic features of apoptosis after acridine orange staining; (2) analysis of DNA fragmentation by (a) agarose gel electrophoresis and (b) fluorescence activated cell sorting (FACS); and (3) viability assays dependent upon mitochondrial function. Induction of fibronectin and beta 3 integrin expression in endothelial cells by VEGF suggests that altered adhesion molecule expression may explain this survival effect.
进行了一系列实验以确定血管内皮生长因子（VEGF）除了具有其内皮细胞特异性促有丝分裂活性外，是否还能保护内皮细胞免受毒素诱导的程序性细胞死亡。用肿瘤坏死因子-α（TNF-α）诱导内皮细胞培养物中的细胞凋亡。当通过以下方法评估时，内皮细胞同时暴露于VEGF导致凋亡的剂量依赖性抑制：（1）吖啶橙染色后直接计数具有凋亡形态特征的细胞；（2）通过（a）琼脂糖凝胶电泳和（b）荧光激活细胞分选（FACS）分析DNA片段化；以及（3）依赖线粒体功能的活力测定。VEGF诱导内皮细胞中纤连蛋白和β3整合素表达，提示粘附分子表达改变可能解释这种存活效应。
