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Platelet Factor 4 Modulates Fibroblast Growth Factor 2 (FGF-2)
Activity and Inhibits FGF-2 Dimerization
Catherine Perollet,
Zhong Chao Han,
Catherine Savona,
Jacques
Philippe Caen, and
Andreas Bikfalvi
From the Growth Factor and Cell Differentiation Laboratory,
University Bordeaux; Institut des Vaisseaux et du Sang, Paris, France;
and Institute of Hematology, Chinese Academy of Medical Science,
Tianjin, China.
Platelet factor 4 (PF-4) inhibits angiogenesis in vitro and in vivo.
The mechanism of inhibition is poorly understood. We have investigated
the mechanism of inhibition by examining the interaction of PF-4 and
the fibroblast growth factor-2 (FGF-2)/fibroblast growth factor
receptor (FGFR) system. PF-4 inhibited the binding of FGF-2 to
high-affinity and low-affinity binding sites in murine microvascular
endothelial cells (LEII cells) and proliferation. Maximum inhibition of
binding to endothelial FGF receptors was observed at PF-4
concentrations between 5 and 10 µg/mL (half maximum inhibition at 0.6 µg/mL), and proliferation was completely inhibited at 2 µg/mL. At
this concentration, PF-4 reduced internalization of
125I-FGF-2 by threefold and delayed degradation. To gain
insight into the mechanism of inhibition, we have analyzed the
interaction of PF-4 with FGF-2/FGFR by using mutant heparan
sulfate-deficient Chinese hamster ovary (CHO) cells
transfected with the FGFR-1 cDNA (CHOm-FGFR-1) and by examining the
direct interaction with FGF-2. In the absence of heparin, PF-4
inhibited binding of 125I-FGF-2 to CHOm-FGFR-1 cells in a
concentration-dependent manner, although not completely. In the
presence of heparin, PF-4 abolished totally the stimulatory effect of
heparin. Furthermore, PF-4 complexed to FGF-2 and inhibited endogenous
or heparin-induced FGF-2 dimerization. These results indicate that PF-4
interacts with FGF-2 by complex formation, inhibiting FGF-2
dimerization, binding to FGF receptors, and internalization. This
mechanism most likely contributes to the antiangiogenic properties of
PF-4.
Blood, Vol. 91 No. 9 (May 1), 1998:
pp. 3289-3299
© 1998 by The American Society of Hematology.
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