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Blood, 15 August 2002, Vol. 100, No. 4, pp. 1334-1339
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Induction of permeability across endothelial cell monolayers by
tumor necrosis factor (TNF) occurs via a tissue factor-dependent
mechanism: relationship between the procoagulant and permeability
effects of TNF
Josef Friedl,
Markus Puhlmann,
David L. Bartlett,
Steven K. Libutti,
Ewa N. Turner,
Michael F. X. Gnant, and
H.
Richard Alexander
From the Surgical Metabolism Section, Surgery Branch,
Center for Cancer Research, National Cancer Institute, Bethesda, MD.
Tumor necrosis factor (TNF) has marked effects on
permeability and procoagulant activity on tumor-associated
neovasculature when used in isolation perfusion, the latter effect
primarily mediated via induction of cell surface expression of tissue
factor (TF) on endothelial tissue. However, the cellular events that result in rapid alterations in endothelial cell (EC) permeability after
intravascular TNF administration in isolation perfusion are not well
characterized. We demonstrate that short exposure intervals to TNF
induces TF expression on ECs but has no effect on permeability as
assessed by flux of Evans blue-bound albumin across confluent EC
monolayers using a 2-compartment model under basal culture conditions.
However, a rapid and significant increase in EC permeability occurred
with TNF in the presence of factor VIII-deficient plasma. Permeability
was induced only with luminal versus abluminal TNF exposure and was
blocked by antithrombin III, TF pathway inhibitor, or anti-TF antibody
cotreatment. These data indicate that EC surface expression of TF and
extrinsic clotting factors are critical in augmenting capillary leak
following intravascular TNF administration. Alterations in permeability
were associated with intercellular gap formation at sites of
down-regulation of vascular endothelial (VE)-cadherin expression, the
primary endothelial intercellular adhesion molecule, and intracellular
contraction and alignment of F-actin cytoskeletal elements. Rapid
induction of TF by TNF may be the primary EC response that results in
alterations in permeability and procoagulant activity observed
following intravascular TNF administration in isolation perfusion.
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