MODULATION OF ENDOTHELIAL CELL HEMOSTATIC PROPERTIES BY TUMOR NECROSIS FACTOR

MODULATION OF ENDOTHELIAL CELL HEMOSTATIC PROPERTIES BY TUMOR NECROSIS FACTOR

March 1986 | BY PETER P. NAWROTH AND DAVID M. STERN
This study investigates the effect of tumor necrosis factor (TNF) on the coagulant properties of endothelial cells. The researchers found that TNF, when incubated with cultured bovine aortic endothelial cells, induced a dose-dependent increase in tissue factor expression, enhancing procoagulant activity. This induction of tissue factor was confirmed by the dependence of Factor X activation on Factor VIIa and the presence of anti-tissue factor IgG. Additionally, TNF suppressed the protein C pathway, an antithrombotic mechanism, by reducing thrombin-mediated protein C activation and the formation of the activated protein C–protein S complex. The results suggest that TNF modulates endothelial cell hemostatic properties, promoting clot formation and potentially contributing to thrombotic states associated with inflammatory and malignant disorders. The findings highlight the role of endothelial cells in the pathogenesis of thrombotic conditions and provide insights into the intercellular signaling mechanisms by which monokines like TNF can influence coagulation.This study investigates the effect of tumor necrosis factor (TNF) on the coagulant properties of endothelial cells. The researchers found that TNF, when incubated with cultured bovine aortic endothelial cells, induced a dose-dependent increase in tissue factor expression, enhancing procoagulant activity. This induction of tissue factor was confirmed by the dependence of Factor X activation on Factor VIIa and the presence of anti-tissue factor IgG. Additionally, TNF suppressed the protein C pathway, an antithrombotic mechanism, by reducing thrombin-mediated protein C activation and the formation of the activated protein C–protein S complex. The results suggest that TNF modulates endothelial cell hemostatic properties, promoting clot formation and potentially contributing to thrombotic states associated with inflammatory and malignant disorders. The findings highlight the role of endothelial cells in the pathogenesis of thrombotic conditions and provide insights into the intercellular signaling mechanisms by which monokines like TNF can influence coagulation.
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