Mice over-expressing placenta growth factor in the skin exhibit increased vascularization and vessel permeability independently of VEGF-A

Placenta growth factor (PlGF), a member of the vascular endothelial growth factor (VEGF) family, shows strong pro-angiogenic properties in adult pathological angiogenesis [1]. In the skin, where keratinocytes represent the major source of VEGF-A and PlGF, these two factors are contemporaneously induced [2,3]. VEGF-A is also expressed in macrophages, and at minimal levels in dermal fibroblasts and endothelial cells; PlGF is also expressed in endothelial cells, at higher levels than VEGF-A. PlGF binds to tyrosine kinase receptor VEGFR-1 (Flt-1), while VEGF-A also binds to VEGFR-2 (Flk-1), which mediates the strongest angiogenic response.