Smooth muscle cells, macrophages, glial cells, keratinocytes, and transformed cells have
been established as synthesis sites for vascular endothelial growth factor (VEGF). The
modulating effects of VEGF are essentially limited to endothelial cells (ECs), the only cell
type consistently shown to express VEGF receptors. VEGF has thus been considered to act
exclusively via a paracrine pathway. We sought to determine whether the role of human ECs
might, under selected conditions, extend beyond that of a target to involve contingency …