The mechanism by which the CXC chemokine platelet fac-tor 4 (PF-4) inhibits endothelial cell proliferation is unclear. The heparin-binding domains of PF-4 have been reported to prevent vascular endothelial growth factor 165 (VEGF165 ) andfibroblast growth factor 2 (FGF2) frominteractingwith their receptors. However, other studies have suggested that PF-4 acts via heparin-binding independent interactions. Here, we compared the effects of PF-4 on the signalling events involved in the proliferation induced by VEGF165 , which binds heparin, and by VEGF121 , which does not
