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Retinoic acid counteracts both the downregulation of thrombomodulin and the
induction of tissue factor in cultured human endothelial cells exposed to
tumor necrosis factor
H Ishii, S Horie, K Kizaki and M Kazama
Department of Clinical Biochemistry, Faculty of Pharmaceutical Sciences,
Teikyo University, Kanagawa, Japan.
Inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha)
shift the hemostatic balance of endothelial cell surfaces in favor of
prothrombotic properties by downregulating thrombomodulin (TM) and inducing
tissue factor (TF) expression. We investigated the effects of retinoic acid
(RA) on the prothrombotic properties of cultured umbilical vein endothelial
cells exposed to TNF-alpha. The approximate 50% downregulation of TM
antigen and cofactor activity induced by TNF- alpha (10 U/mL for 24 hours)
was completely prevented when the cells were coincubated with both
TNF-alpha and 10 mumol/L RA. In accordance with changes in cell surface TM
antigen levels, the 70% decrease in TM messenger RNA (mRNA) induced by
TNF-alpha was also prevented by 10 mumol/L RA. TNF-alpha induced TF
activity of lysed cells (100-fold greater than untreated controls), an
effect prevented when the cells were coincubated with both the TNF-alpha
and 10 mumol/L RA. The 34-fold increase in TF mRNA levels induced by
TNF-alpha (10 U/mL for 3 hours) was only two-fold in the presence of both
TNF-alpha and RA. The effects of RA on the regulation of TM and TF
expression in the cells exposed to TNF-alpha was dose-dependent from 0.01
to 10 mumol/L RA. The present results suggest that RA may affect on the
mRNA level to alter TM and TF expression, effectively counteracting
expression of prothrombotic properties of endothelial cells induced by
inflammatory cytokines such as TNF-alpha.
Volume 80,
Issue 10,
pp. 2556-2562,
11/15/1992
Copyright © 1992 by The American Society of Hematology
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