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Plasminogen activator inhibitor-1 messenger RNA expression is induced in
rat hepatocytes in vivo by dexamethasone
BA Konkle, SJ Schuster, MD Kelly, K Harjes, DE Hassett, M Bohrer and M Tavassoli
Department of Medicine, Jefferson Medical College, Thomas Jefferson
University, Philadelphia, PA 19107.
Plasminogen activator inhibitor-1 (PAI-1), the major physiologic inhibitor
of tissue plasminogen activator (tPA), plays a crucial role in the
regulation of fibrinolysis. Both hepatocytes and endothelial cells have
been implicated as major sources of plasma PAI-1. To study the relative
contribution of these cell types to hepatic PAI-1 production, we have
separated hepatocytes and hepatic sinusoidal endothelial cells by
fractionation of freshly isolated rat livers using metrizamide density
gradients and centrifugal elutriation. In untreated animals, PAI-1
messenger RNA (mRNA) was detected only in the purified endothelial cell
fraction, and not in the hepatocyte fraction or in unfractionated liver.
However, when the animals were treated with dexamethasone, PAI-1 mRNA
expression was transiently induced in the liver. This induction paralleled
the appearance of PAI-1 mRNA in purified hepatocytes, while PAI-1
expression in sinusoidal endothelial cells was unchanged. Four hours after
dexamethasone treatment, plasma PAI-1 levels were increased approximately
twofold over levels measured in animals treated with the diluent alone.
These data suggest that PAI- 1 production by hepatocytes may contribute to
elevated plasma PAI-1 levels in the setting of acute injury and stress.
Volume 79,
Issue 10,
pp. 2636-2642,
05/15/1992
Copyright © 1992 by The American Society of Hematology
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