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Cytokine treatment of endothelial cells increases glycoprotein Ib alpha-
dependent adhesion to von Willebrand factor
DA Beacham, LP Tran and SS Shapiro
The Cardeza Foundation for Hematologic Research, Department of Medicine,
Jefferson Medical College of Thomas Jefferson University, Philadelphia, PA
19107-5099, USA.
Endothelial cells (EC) possess at least two membrane receptors for von
Willebrand factor (vWF), the vitronectin receptor (VNR, alpha(v)beta3),
which recognizes an Arg-Gly-Asp (RGD) sequence in the C-terminus of vWF,
and glycoprotein Ib alpha (GP Ib alpha), which interacts with a region in
the N-terminal A1 domain of vWF. In the absence of added cytokines, EC
attachment to a vWF substratum is mediated largely through the
alpha(v)beta3, with a smaller contribution by GP Ib alpha. In the present
study, we have examined the effect of cytokines on the receptor specificity
of EC attachment to wild-type vWF (WT-vWF) and to vWF, which had been
mutated in the C-terminal RGDS sequence (RADS-vWF). Exposure of human
umbilical vein EC (HUVEC) to tumor necrosis factor- alpha (TNF-alpha) or to
TNF-alpha in combination with interferon-gamma (IFN-gamma), but not to
interleukin-1beta (IL-1), increased attachment to RADS-vWF by about
twofold. The TNF-alpha-induced increase in EC attachment was accompanied by
an increase in cell surface GP Ib alpha expression; GP Ib alpha surface
expression was not increased by IL-1. Attachment of untreated HUVEC to
WT-vWF could be inhibited 60% to 70% by a monoclonal antibody (MoAb)
(LM609) to the VNR and 30% to 40% by the A1 fragment of vWF (containing the
GP Ib alpha binding domain). The pattern of inhibition of attachment to
WT-vWF was largely unchanged after TNF-alpha treatment of HUVEC. In
contrast, the attachment to WT- vWF of HUVEC, treated with TNF-alpha
+IFN-gamma was completely inhibited by vWF-A1 and inhibited only 35% by the
anti-VNR antibody LM609. Two MoAbs to GP Ib alpha produced similar, but
incomplete, inhibition. Pretreatment of HUVEC with the combination of
TNF-alpha + IFN-gamma produced a dramatic decrease in VNR expression,
confirming previous findings of Defilippi et al. These results suggest that
in the presence of the inflammatory cytokines TNF-alpha + IFN-gamma, the
endothelial GP Ib complex is a major determinant of HUVEC adhesion to
surface-bound vWF.
Volume 89,
Issue 11,
pp. 4071-4077,
06/01/1997
Copyright © 1997 by The American Society of Hematology
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