Cao Y, Linden P, Shima D, Browne F, Folkman J
Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115, USA.
J Clin Invest. 1996 Dec 1;98(11):2507-11. doi: 10.1172/JCI119069.
To investigate the in vivo angiogenic activity of placenta growth factor (PIGF) and its heterodimers with vascular endothelial growth factor (VEGF), the induction of neovascularization of these factors in the mouse cornea was studied. VEGF165 is sufficiently potent to stimulate new capillary growth from the limbal vessels. PIGF129/VEGF165 heterodimers also induce corneal neovascularization with a maximal vessel length similar to VEGF165, but with a marked decrease of vessel density. In contrast, PIGF129 has little or no effect in this in vivo angiogenesis assay. The expression of VEGF mRNA and protein is drastically up-regulated by hypoxia in choriocarcinoma cells, whereas expression of PIGF is not affected by the low concentration of oxygen. Up-regulation of VEGF production results in increased formation of PIGF/VEGF heterodimers in these tumor cells. Thus, hypoxia indirectly up-regulates expression levels of PIGF/VEGF heterodimers and modulates VEGF activity when these factors are co-expressed.
为了研究胎盘生长因子(PIGF)及其与血管内皮生长因子(VEGF)的异二聚体在体内的血管生成活性,我们研究了这些因子在小鼠角膜中诱导新生血管形成的情况。VEGF165有足够的能力刺激来自角膜缘血管的新毛细血管生长。PIGF129/VEGF165异二聚体也能诱导角膜新生血管形成,其最大血管长度与VEGF165相似,但血管密度显著降低。相比之下,PIGF129在这种体内血管生成试验中几乎没有作用或没有作用。在绒毛膜癌细胞中,缺氧会显著上调VEGF mRNA和蛋白的表达,而PIGF的表达不受低氧浓度的影响。VEGF产生的上调导致这些肿瘤细胞中PIGF/VEGF异二聚体形成增加。因此,当这些因子共同表达时,缺氧会间接上调PIGF/VEGF异二聚体的表达水平并调节VEGF活性。