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and IFN-
in rat aortic smooth muscle cells
Vascular Biology Center and Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912-2500
In rat aortic smooth muscle cells
(RASMC), interferon (IFN)-
enhanced nitrite accumulation and type II
nitric oxide synthase (iNOS) protein expression induced by interleukin
(IL)-1
. IFN- alone had no effect on nitrite accumulation or iNOS
protein. IL-1, but not IFN-, induced nuclear factor (NF)-
B and
CCAAT box/enhancer binding protein (C/EBP) nuclear binding. Conversely,
IFN-, but not IL-1, induced signal transducer and activator of
transcription (STAT) 1 and interferon regulatory factor (IRF)-1
binding. In a 
1.4-kb rat iNOS promoter segment, deletion of an
IFN--activated site (GAS) increased IL-1-induced activity but
inhibited IFN--enhanced activity, suggesting a two-way effect of the
GAS site on iNOS induction: enhancing induction through STAT1
activation and inhibiting induction through a non-IFN--mediated
mechanism. Deletion of both an IRF and a C/EBP site reduced the
IL-1-induced and the IFN--enhanced activities. However, IRF site
mutations decreased the IFN--enhanced activity without affecting the
IL-1-induced activity. Insertion of two IRF sites increased the
IFN--enhanced, but not the IL-1-induced, activity. Mutations of a
reverse NF-B site did not significantly change IFN--enhanced
activity. We conclude that in RASMC, NF-B and C/EBP mediate the
IL-1-induced iNOS expression, whereas IRF-1 and STAT1 mediate the
IFN--enhanced iNOS induction.
nuclear factor-B; CCAAT box/enhancer binding protein; interferon
regulatory factor-1; signal transducer and activator of transcription
1; interferon- activation site
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