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Tumor necrosis factor alpha is involved in the induction of plasminogen activator inhibitor-1 by endotoxin

M Yamashita1, M Yamashita

  • 1Department of Emergency Medicine, University of Tsukuba, Japan.

Thrombosis Research
|July 15, 1997
PubMed

Treatment with endotoxin leads to a rise in plasminogen activator inhibitor-1 (PAI-1) both in vivo and in vitro. Although a recent study insists that inhibition of tumor necrosis factor alpha (TNF alpha) does not reduce the induction of PAI-1 by endotoxin in rats, we imagine that TNF alpha is involved in the induction of PAI-1 by endotoxin, because endotoxin treatment induces TNF alpha and administration of TNF alpha induces PAI-1 both in vitro and in vivo. In order to confirm this hypothesis, we have measured plasma PAI activity and PAI-1 mRNA in liver after endotoxin treatment with or without pretreatment by polyclonal rabbit antiserum against murine TNF alpha. Chronically cannulated Sprague-Dawley rats received intravenous injection of endotoxin (10 micrograms/kg) 10 min after administration of anti-TNF alpha antibody (Antibody Group) or same volume of control rabbit serum (Control Group). PAI activity was measured by Coatest PAI, and PAI-1 mRNA was measured semi-quantitatively by high-performance liquid chromatography after reverse transcription and polymerase chain reaction. Increases in PAI activity 4 h after endotoxin treatment were significantly smaller in the Antibody Group than in the Control Group, while increases in PAI-1 mRNA were significantly smaller at 2 h in the Antibody Group. These results suggest that TNF alpha is responsible, at least in part, for the induction of PAI-1 by endotoxin in vivo.

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