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Tumor necrosis factor leads to the internalization and degradation of
thrombomodulin from the surface of bovine aortic endothelial cells in
culture
KL Moore, CT Esmon and NL Esmon
Department of Medicine, Indiana University School of Medicine,
Indianapolis.
Tumor necrosis factor (TNF), a mediator of the inflammatory response,
induces tissue factor and decreases the expression of thrombomodulin (TM)
on endothelial cells, thus shifting the hemostatic properties of the
endothelium. To determine the mechanism of TM downregulation, bovine aortic
endothelial cells in culture were treated with TNF (2 nmol/L) and the fate
of TM followed. Both surface expressed TM (antigen and activity), and the
total TM pool (measured by radioimmunoassay and activity in detergent
extracts) dropped to less than or equal to 20% of control values within 12
hours of TNF treatment. TM was not found in an immunologically recognizable
form in the supernatants of treated cultures. Chloroquine (greater than or
equal to 100 mumol/L) was able to abrogate the TNF effect on the total TM
pool but not the effect on surface-expressed TM activity. We conclude that
TNF induces the internalization and subsequent degradation of the TM
molecule. None of the components of the protein C anticoagulant pathway,
either alone or in combination, prevented the TNF-dependent downregulation
of TM antigen.
Volume 73,
Issue 1,
pp. 159-165,
01/01/1989
Copyright © 1989 by The American Society of Hematology
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