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J. Biol. Chem., Vol. 275, Issue 21, 16390-16399, May 26, 2000
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From the Department of Medicine, University of California San
Francisco, Metabolism Section, Medical Service, Department of Veterans
Affairs Medical Center, San Francisco, California 94121
The acute phase response (APR) is associated with
decreased hepatic expression of many proteins involved in lipid
metabolism. The nuclear hormone receptors peroxisome
proliferator-activated receptor
The Acute Phase Response Is Associated with Retinoid X
Receptor Repression in Rodent Liver*
(PPAR) and liver X receptor
(LXR) play key roles in regulation of hepatic lipid metabolism. Because
heterodimerization with RXR is crucial for their action, we
hypothesized that a decrease in RXR may be one mechanism to
coordinately down-regulate gene expression during APR. We demonstrate
that lipopolysaccharide (LPS) induces a rapid,
dose-dependent decrease in RXR, RXR
, and RXR
proteins in hamster liver. Maximum inhibition was observed at 4 h
for RXR (62%) and RXR (50%) and at 2 h for RXR (61%). These decreases were associated with a marked reduction in RXR, RXR, and RXR mRNA levels. Increased RNA degradation is likely responsible for the repression of RXR, because LPS did not decrease RXR and RXR transcription and only
marginally inhibited (38%) RXR transcription. RXR
repression was associated with decreased LXR and PPAR mRNA
levels and reduced RXR·RXR, RXR·PPAR and RXR·LXR binding
activities in nuclear extracts. Furthermore, LPS markedly decreased
both basal and Wy-14,643-induced expression of acyl-CoA synthetase, a
well characterized PPAR target. The reduction in hepatic RXR levels
alone or in association with other nuclear hormone receptors could be a
mechanism for coordinately inhibiting the expression of multiple genes
during the APR.
*
This work was supported by grants from the Research Service
of the Department of Veterans Affairs and by National Institutes of
Health Grants DK 49448 and AR 39639.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Veterans
Affairs Medical Center, Metabolism Section (111F), 4150 Clement St.,
San Francisco, CA 94121. Tel.: 415-750-2005; Fax: 415-750-6927; E-mail: kfngld@itsa.ucsf.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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