Role of vascular endothelial growth factor in the response to vessel injury

Abstract

Role of vascular endothelial growth factor in the response to vessel injury. In the post-embryonic life, physiological angiogenesis is tightly controlled. Angiogenesis also occurs in pathological circumstances such as tumor vessel proliferation, retinal neovascularization and ischemia. The development of collateral circulation is not only not deleterious, but life saving. Other cases such as neoplastic neovascularization are the basis of the continuous growth of tumors and metastases, and therefore constitute a target of therapeutical efforts. Among a list of molecules able to control angiogenesis, we emphasize the pivotal role of vascular endothelial growth factor (VEGF). VEGF is a potent mitogen for endothelial cells, but is devoid of mitogenic activity for other cell types. VEGF is a polypeptide with four main different isoforms that are remarkably different in terms of solubility and affinity for matrix proteins. VEGF interacts with two endothelial cell-specific tyrosine kinase receptors. The main interest of its study lies in VEGF's role in pathological angiogenic processes, where an increase in the VEGF mRNA expression has been consistently observed. An interesting example is the up-regulation of VEGF's and VEGF receptors' mRNA in a considerable number of human tumors and retina, where they have a critical role in the development of neovascularization. In recent work in our laboratory, we have found further potential interactions of VEGF with pathophysiological mechanisms, namely, the increase in VEGF gene expression under exposure to reactive oxygen species and the positive interaction between VEGF and erythropoietin. VEGF has outstanding possibilities for therapeutic applications aimed at inhibiting or favoring the development of new vessels.

Expression of vascular endothelial growth factor receptors and their ligands in rat uterus during the postpartum involution period

“…We observed strong VEGF immunoreactivity in the endothelial cells during days 1, 3 and 5 of the PP, and weak immunoreactivity during days 10 and 15 of the PP. By contrast to our fi ndings, earlier reports indicated that VEGF is expressed in vascular smooth muscle cells and that it is overexpressed as a result of injury factors including hypoxia or mechanical injury (Kuroki et al 1996, Alvarez-Arroyo et al 1998.…”

Rosiglitazone attenuates hypoxia‐induced pulmonary arterial hypertension in rats

“…Vascular endothelial growth factor is a chemotactic factor for monocytes, macrophages and vascular endothelial cells, and expression of VEGF is regulated by hypoxia, IL‐1, IL‐6, insulin‐like growth factor‐1 and transforming growth factor‐β 25–27 . VEGF may have an important role in the pathogenesis of pulmonary hypertension, although some studies have implicated VEGF in attenuating the development of pulmonary hypertension 28 .…”

Dual Role of VEGF in Pretreated Experimental ePTFE Arterial Grafts

“…VEGF is produced by fibroblasts, SMC, and EC. It may be overexpressed upon the influence of several injuring factors like trauma, hypoxia, and reactive oxygen species [25,26]. VEGF has been shown to promote angiogenesis in vitro and in vivo [27,28].…”