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Blood, 15 November 2000, Vol. 96, No. 10, pp. 3466-3472
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Interleukin 1 inhibits interleukin 6-mediated rat  fibrinogen gene expression
Zhixin Zhang and
Gerald M. Fuller
From the Department of Cell Biology, University of
Alabama at Birmingham, Birmingham, AL.
Interleukin (IL)-1 and IL-6 are the 2 major inducers of a group
of hepatic genes during acute inflammation; however, each cytokine uses
different intracellular signaling molecules. In most instances, the 2 cytokines interact positively to enhance hepatic gene expression, but
in one class of acute-phase reactants, which includes fibrinogen,
IL-1 exerts a transient inhibitory effect over the IL-6 stimulatory
signal. This study explored the effects of IL-1/nuclear factor  B
(NF-B) and IL-6/signal transducer and activator of transcription 3 (STAT3) combinatory signaling on the transcriptional regulation of the
rat  fibrinogen gene. Northern blot and functional analyses
employing luciferase reporter constructs driven by the rat fibrinogen promoter demonstrated that IL-1 inhibited the
IL-6-mediated transcription of this gene. Exposing primary rat
hepatocytes to IL-1 had no effect on IL-6-mediated STAT3 activation;
instead, IL-1-activated NF-B associated with 2 IL-6 responsive
elements (STAT3 binding site) on the rat fibrinogen promoter and
blocked STAT3 binding to these regions. The competitive binding of
NF-B and STAT3 on the overlapping binding site provides a mechanism
for the inhibition by IL-1 of the IL-6-mediated transactivation of
rat fibrinogen.
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