Interleukin 1 stimulates endothelial cell tissue factor production and expression by a prostaglandin-independent mechanism.
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.
D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004727:Endothelium / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology*; D011453:Prostaglandins / Q000502:physiology*; D011956:Receptors, Cell Surface / Q000187:drug effects; D013923:Thromboembolism / Q000209:etiology; D013925:Thromboplastin / Q000096:biosynthesis*; D013997:Time Factors
D007375:Interleukin-1; D011453:Prostaglandins; D011956:Receptors, Cell Surface; D013925:Thromboplastin