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Migration of human monocytes in response to vascular endothelial growth
factor (VEGF) is mediated via the VEGF receptor flt-1
B Barleon, S Sozzani, D Zhou, HA Weich, A Mantovani and D Marme
Institute of Molecular Medicine, Tumor Biology Center Freiburg, Germany.
Treatment of human monocytes with vascular endothelial growth factor (VEGF)
isolated from tumor cell supernatants was reported to induce monocyte
activation and migration. In this study we show that recombinant human
VEGF165, and VEGF121 had a maximal effect on human monocyte migration at 65
to 250 pmol/L. Chemotactic activity of VEGF165 was inhibited by a specific
antiserum against VEGF, by heat treatment of VEGF165, and by protein kinase
inhibitors. In addition, we could show that VEGF-stimulated monocyte
migration is mediated by a pertussis toxin-sensitive GTP-binding protein.
Placenta growth factor (PlGF152), a heparin-binding growth factor related
to VEGF, was also chemotactic for monocytes at concentrations between 2.5
and 25 pmol/L. In accordance with these findings, human monocytes showed
specific and saturable binding for 125I-VEGF165 (half-maximal binding at 1
to 1.5 nmol/L). Using Northern blot analysis, we further could show that
human monocytes express only the gene for the VEGF receptor type, flt-1,
but not for the second known VEGF receptor, KDR. Resting monocytes
expressed low levels of flt-1 gene only. Brief exposure (2 to 4 hours) of
human monocytes to lipopolysaccharide, a prototypic monocyte activator, led
to a significant upregulation of the flt-1 mRNA level. The results
presented here suggest that monocyte chemotaxis in response to VEGF and
most likely to PlGF152 is mediated by flt-1 and thus show a possible
function for the VEGF-receptor flt-1.
Volume 87,
Issue 8,
pp. 3336-3343,
04/15/1996
Copyright © 1996 by The American Society of Hematology
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