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Both tumor necrosis factor receptors, TNFR60 and TNFR80, are involved in
signaling endothelial tissue factor expression by juxtacrine tumor necrosis
factor alpha
EF Schmid, K Binder, M Grell, P Scheurich and K Pfizenmaier
Department of Pharmacological Research, Dr Karl Thomae GmbH, Biberach,
Germany.
We have investigated the role of the two distinct tumor necrosis factor
(TNF) receptors (TNFR60 and TNFR80) in endothelial cell activation
employing an in vitro model of tumor necrosis factor alpha (TNF-alpha)-
dependent tissue factor production of human umbilical vein endothelial
cells (HUVECs). In this model, tissue factor is produced either on addition
of exogeneous TNF-alpha, or by induction of endogenous TNF- alpha via
adhesion molecule-linked signal pathways. Under both conditions, tissue
factor expression could be partially blocked by antagonistic antibodies
against either TNFR60 or TNFR80 and was fully inhibited by simultaneous
application of both antibodies. Selective inhibitors of either TNFR60 or
TNFR80-induced signal pathways inhibited tissue factor expression, and
selective triggering of either of the two TNF receptors by agonistic
antibodies induced this response in HUVECs. Furthermore, a coculture system
of HUVECs and Chinese hamster ovary transfectants expressing a
noncleavable, exclusively membrane-bound form of TNF-alpha resulted in a
potent activation of HUVECs with synergistic action of both TNF receptors.
Together, these data underline the importance of juxtacrine pathways in
endothelial cell activation of procoagulant functions and show that
membrane TNF-alpha and both TNFR types play a critical role.
Volume 86,
Issue 5,
pp. 1836-1841,
09/01/1995
Copyright © 1995 by The American Society of Hematology
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