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B,
and CREB in the lungs after hemorrhage and
endotoxemia
Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262
The transcriptional regulatory
factor nuclear factor (NF)-
B has a central role in modulating
expression of proinflammatory mediators that are important in acute
lung injury. In vitro studies have shown that competition between
NF-B and cAMP response element binding protein (CREB) for binding to
the coactivator CREB-binding protein (CBP) is important in regulating
transcriptional activity of these factors. In the present study, we
examined in vivo interactions between CBP, CREB, and NF-B in
hemorrhage- or endotoxemia-induced acute lung injury. Association of
CBP with CREB or the p65 subunit of NF-B increased in the lungs
after hemorrhage or endotoxemia. Inhibition of xanthine oxidase before
hemorrhage, but not before endotoxemia, decreased p65-CBP interactions
while increasing those between CREB and CBP. These alterations in
CREB-CBP and p65-CBP interactions were functionally significant because
xanthine oxidase inhibition before hemorrhage resulted in increased
expression of the CREB-dependent gene c-Fos and decreased expression of
macrophage inflammatory protein-2, a NF-B-dependent gene. The
present results show that the coactivator CBP has an important role in
modulating transcription in vivo under clinically relevant
pathophysiological conditions.
acute lung injury; inflammation; gene expression regulation; transcription factors; reactive oxygen species; adenosine 3'5'-cyclic
monophosphate response element binding protein binding protein; nuclear
factor-B
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