Tumor necrosis factor/cachectin-induced modulation of endothelial cell hemostatic properties.
Tumor necrosis factor/cachectin (TNF) is a mediator of the septic shock state, which can modulate hemostatic properties of the vessel wall. The interaction of TNF with endothelium is not cytotoxic, rather it is receptor mediated and results in a change in receptor expression on the endothelial cell surface, enabling endothelium to actively promote coagulation. Anticoagulant mechanisms, including the protein C/protein S system and fibrinolysis are suppressed, whereas the initiation and propagation of procoagulant activity is enhanced. This unidirectional shift in vessel wall coagulant activity favoring clot formation could contribute to the coagulopathy associated with sepsis and indicates a mechanism through which the coagulation system serves as an integral part of the host response.
Nawroth
P P
PP
Oklahoma Medical Research Foundation, Oklahoma City.
Stern
D M
DM
D000818:Animals; D004211:Disseminated Intravascular Coagulation / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006487:Hemostasis; D006801:Humans; D009374:Neoplasms, Experimental / Q000503:physiopathology; D011956:Receptors, Cell Surface / Q000502:physiology; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
D011956:Receptors, Cell Surface; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha