Summary
Activation of coagulation occurs at inflammatory sites following the ingress of mononuclear
cells, and may result from alterations in the vessel wall. Since the monokine, interleukin
1, initiates diverse responses to inflammation, its ability to enhance vascular procoagulant
activity was studied. Interleukin 1-treated cultured human endothelial cells acquired
elevated levels of the procoagulant, tissue factor. This required de novo protein
synthesis, was maximal at 2 h after exposure to interleukin 1, and resulted in persistently
elevated cellular procoagulant activity. Tissue factor was later expressed (6-24 h)
on the surface of uninjured endothelial cells. Endothelial cell procoagulant production
and expression in response to interleukin 1 could be dissociated from endogenous prostaglandin
metabolism, being insensitive to hydrocortisone, indomethacin, eicosatetrayionic acid
and exogenous arachidonic acid. In addition, no increase in prostaglandin synthesis
occurred during the interval in which tissue factor was synthesized. We therefore
conclude that interleukin 1 stimulates endothelial synthesis and surface expression
of tissue factor by a prostaglandin-independent mechanism.
Key words
Endothelial cells - Interleukin 1 - Prostacyclin - Thrombogenicity - Tissue factor
