Asahara T, Takahashi T, Masuda H, Kalka C, Chen D, Iwaguro H, Inai Y, Silver M, Isner J M
Departments of Medicine (Cardiology) and Biomedical Research, St Elizabeth's Medical Center, Tufts University School of Medicine, 736 Cambridge Street, Boston, MA 02135, USA.
EMBO J. 1999 Jul 15;18(14):3964-72. doi: 10.1093/emboj/18.14.3964.
Vascular endothelial growth factor (VEGF) has been shown to promote neovascularization in animal models and, more recently, in human subjects. This feature has been assumed to result exclusively from its direct effects on fully differentiated endothelial cells, i.e. angiogenesis. Given its regulatory role in both angiogenesis and vasculogenesis during fetal development, we investigated the hypothesis that VEGF may modulate endothelial progenitor cell (EPC) kinetics for postnatal neovascularization. Indeed, we observed an increase in circulating EPCs following VEGF administration in vivo. VEGF-induced mobilization of bone marrow-derived EPCs resulted in increased differentiated EPCs in vitro and augmented corneal neovascularization in vivo. These findings thus establish a novel role for VEGF in postnatal neovascularization which complements its known impact on angiogenesis.
血管内皮生长因子（VEGF）已被证明在动物模型中能促进新血管形成，最近在人体中也有此作用。人们认为这一特性完全是其对完全分化的内皮细胞的直接作用所致，即血管生成。鉴于其在胎儿发育过程中对血管生成和血管发生的调节作用，我们研究了VEGF可能调节内皮祖细胞（EPC）动力学以促进出生后新血管形成的假说。事实上，我们观察到在体内给予VEGF后循环EPCs增加。VEGF诱导的骨髓源性EPCs动员导致体外分化的EPCs增加，并增强了体内角膜新血管形成。因此，这些发现确立了VEGF在出生后新血管形成中的新作用，这补充了其对血管生成的已知影响。
