Cardiovascular Research vol:86 issue:1 pages:29-36
Aims: The vascular endothelial growth factor homologue placental growth factor (PlGF) is a
pleiotropic cytokine, with a pro-inflammatory activity. Previous gene-inactivation studies
revealed that loss of PlGF delays atherosclerotic lesion development and inhibits macrophage
infiltration, but the activity of an anti-PlGF antibody (aPlGF mAb) has not been evaluated yet.
Methods and Results: We characterized the potential of short-term delivery of aPlGF mAb in
inhibiting lesion development in ApoE-deficient mice (apoE-/-) and in CD4:TGFßRIIDN x apoE-/-
mice, a more severe atherosclerosis model. Short-term treatment of aPlGF mAb reduces
early atherosclerotic plaque size and inflammatory cell infiltration in the lesion.
Conclusions: These pharmacological aPlGF mAb results confirm previous genetic evidence
that inhibition of PlGF slows down early atherosclerotic lesion development. Furthermore, the
phenocopy of genetic and pharmacological loss-of-function strategies underscores that
aPlGF acts by selectively neutralizing PlGF.