VEGF stimulated the angiogenesis by promoting the mitochondrial functions.

The vascular endothelial growth factor (VEGF) signaling pathway involved in angiogenesis which plays a pivotal role in normal development and also represents a major therapeutic target for tumors and intraocular neovascular disorders. The aims of the present study were to evaluate the effects of VEGF on endothelial cells and clarify the mechanism. Here, we showed that VEGF significantly stimulated the proliferation, migration and cell cycle of endothelial cells, and it also induced tube formation significantly. What's more, the mitochondrial functions were enhanced in response to VEGF, including mitochondrial oxidative respiration and intracellular ATP levels. The reactive oxygen species (ROS) production decreased, while the enzymes of ROS defence system, including catalase and glutathione peroxidase (GPX1), whose expression both increased in the VEGF stimulation. VEGF activated mammalian target of rapamycinm (mTOR) signaling pathway to promote the function of mitochondria. Rapamycin, the inhibitor of mTOR pathway could inhibit the proliferation and cell cycle induced by VEGF. In summary, our study identified that VEGF promoted the angiogenesis and provided evidence for mitochondria as new therapeutic target of VEGF signaling in the angiogenic vascular disorders.