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Department of Anesthesiology, University of Illinois at Chicago, Chicago, Illinois 60612, USA
1Correspondence: Anesthesiology M/C519, University of Illinois at Chicago, 1819 W. Polk St., Chicago, IL 60612, USA. E-mail: egalea{at}uic.edu
The enzyme nitric oxide synthase 2 (NOS2), often called inducible NOS,
plays a central role in the inflammatory reactions that follow
infection or tissue damage. NOS2 has been detected in virtually every
cell type, and the NO it produces can perform both beneficial and
detrimental actions. It is thus conceivable that regulatory mechanisms
exist which control the timing and intensity of NO production by NOS2
in order to outweigh protective effects against detrimental ones. Since
cyclic AMP inhibits numerous immunological reactions, studies have been
carried out to determine whether cAMP-dependent pathways could inhibit
NOS2 expression as well. Pharmacological studies in cultured cells show
that, depending on the cell type examined, increased cAMP can exert
opposite effects on the endotoxin- or cytokine-induced expression of
NOS2, being either stimulatory or inhibitory in macrophages,
stimulatory in adipocytes, smooth muscle, skeletal muscle, and brain
endothelial cells, and inhibitory in pancreatic, liver, and brain glial
cells. Regulation of NOS2 gene transcription appears to be the primary
mechanism of action of cAMP, and whether it is stimulatory or
inhibitory hinges on the cell-specific regulation of transcription
factors including CREB, NF-
B, and C/EBP. Cyclic AMP must therefore
be considered a modulator rather than a suppressor of NOS2 expression.
This review summarizes evidence derived from in vitro
studies, considers regulation of NOS2 by cAMP in vivo,
and discusses possible therapeutic applications of cAMP
treatment.—Galea, E., Feinstein, D. L. Regulation of the
expression of the inflammatory nitric oxide synthase (NOS2) by cyclic
AMP.
Key Words: transcription factors • gene expression • promoter • gene structure • mRNA expression • cytokines • endotoxin
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