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Endotoxin-induced tissue factor messenger RNA in human monocytes is
negatively regulated by a cyclic AMP-dependent mechanism
V Ollivier, S Houssaye, C Ternisien, A Leon, H de Verneuil, C Elbim, N Mackman, TS Edgington and D de Prost
Service d'immunologie et d'hematologie, CHU Xavier Bichat, Paris, France.
Tissue factor (TF) is a transmembrane receptor that serves as the major
cofactor for factor VIIa-catalyzed proteolytic activation of factors IX and
X. In response to bacterial lipopolysaccharide (LPS), monocytes transcribe,
synthesize, and express TF on their surface, thereby conveying to activated
monocytes the ability to initiate the blood coagulation protease cascades.
Agents that elevate cellular cyclic AMP (cAMP) inhibit the functional
expression of TF by LPS-stimulated monocytes. In this study, we
investigated the mechanism of this suppression. Northern blot analysis of
total RNA from LPS-stimulated monocytes showed a concentration-dependent
decrease in TF messenger RNA (mRNA) levels in response to dibutyryl-cAMP
(dBt-cAMP). TF mRNA and procoagulant activity were inhibited as early as 1
hour after the addition of dBt-cAMP and the inhibition persisted through 4
hours. Suppression of specific mRNA abundance was also observed with
agents, including forskolin and iso-butyl-methyl-xanthine (IBMX), that
increase cAMP levels by independent mechanisms. Flow immunocytometric
analysis confirmed that cell-surface TF protein levels declined in parallel
with TF functional activity. The rate of decay of TF mRNA after the arrest
of transcription by actinomycin D was not altered by the addition of
dBt-cAMP, IBMX, or forskolin, thus excluding effects on TF mRNA stability.
We conclude that elevated cAMP levels suppress TF mRNA by reducing the rate
of TF gene transcription.
Volume 81,
Issue 4,
pp. 973-979,
02/15/1993
Copyright © 1993 by The American Society of Hematology
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