VEGF (known also as VEGFA) was initially identified in conditioned medium from bovine pituitary follicular cells. VEGFA belongs to the VEGF family, which has the following members: VEGF-A, VEGF-B, VEGF-C (VEGF-2), VEGF-D, and PlGF (placental growth factor). In addition, viral VEGF homologs (collectively called VEGF-E) and snake venom VEGFs, such as T.f. (Trimeresurus flavoviridis) and svVEGF (called VEGF-F), have been described. VEGFA is alternatively spliced to generate variants with different numbers of amino acids, such as VEGFA121, VEGFA145, VEGFA165, and VEGFA189. VEGFA165 is predominant and responsible for VEGFA biological potency. While VEGF121 is freely diffusible and does not bind to neuropilins (NRPs) or heparan sulphate (HS), VEGF165 and VEGF189 bind to both, resulting in retention on the cell surface or in the extracellular matrix. NRP1 lacks a typical kinase domain and acts as a co-receptor, and in response to VEGF165, NRP1 couples with VEGF-Rs to signal in endothelial cells. In addition, it has been suggested that bone marrow cells that are recruited to Ewing’s tumors are differentiated into vascular smooth muscle cells, and VEGF165 is responsible for this differentiation. VEGFA is highly expressed in most of the solid tumors generated in breast, lung, renal, colorectal, and liver tissues. VEGFA has strong vascular permeability activity, and significantly contributes to the formation of ascites tumors. VEGFA can act as a direct proinflammatory mediator during the pathogenesis of rheumatoid arthritis (RA), and protect rheumatoid synoviocytes from apoptosis, which contributes to synovial hyperplasia. VEGFA is expressed in synovial macrophages and synovial fibroblasts in RA patients. Also, VEGFA is associated to age-related macular degeneration (AMD). AMD is due to neovascularization that originates from endothelial cells in the choroid that grow into neurosensory retina as choroidal neovascularization (CNV).
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