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J. Biol. Chem., Vol. 275, Issue 29, 21805-21808, July 21, 2000
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From the Mammalian Cell and Molecular Biology Laboratory, San
Diego State University, San Diego, California 92182-4614
In the studies reported herein, we
show that two complementary experimental models: inbred strains of mice
(i.e. C57BL/6 and C3H/HeJ), and a differentiated line of
rat hepatoma cells (i.e. L35 cells), require the activation
of cytokines by monocyte/macrophages to display bile acid negative
feedback repression of cholesterol 7
ACCELERATED PUBLICATION
Bile Acid Induction of Cytokine Expression by Macrophages
Correlates with Repression of Hepatic Cholesterol 7
-Hydroxylase*
,, and
-hydroxylase (CYP7A1). Feeding a
bile acid-containing atherogenic diet for 3 weeks to C57BL/6 mice led
to a 70% reduction in the expression of hepatic CYP7A1 mRNA,
whereas no reduction was observed in C3H/HeJ mice. The strain-specific
response to repression of CYP7A1 paralleled the activation of hepatic
cytokine expression. Studies using cultured THP-1 monocyte/macrophages
showed that the hydrophobic bile acid chenodeoxycholate, a well
established potent repressor of CYP7A1, induced the expression of
mRNAs encoding interleukin 1 (IL-1) and tumor necrosis factor (TNF). In contrast, the hydrophilic bile acid ursodeoxycholate,
which does not repress CYP7A1, did not induce cytokine mRNA
expression by THP-1 cells. Chenodeoxycholate activation of cytokines by
THP-1 cells was blocked by the peroxisome proliferator-activated
receptor 
agonist rosiglitazone. The expression of cytokines
(e.g. IL-1 and TNF) by THP-1 cells paralleled with the
ability of these cells to produce conditioned medium that when added to
rat L35 hepatoma cells, repressed CYP7A1. Moreover, rosiglitazone,
which blocks cytokine activation by macrophages, also blocked the
repression of CYP7A1 normally exhibited by C57BL/6 mice fed the bile
acid-containing atherogenic diet. The combined data indicate that the
activation of cytokines may mediate CYP7A1 repression caused by feeding
mice an atherogenic diet containing bile acids.
*
This work was supported by National Institutes of Health
Grants HL57974 and HL57974.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.
Each author contributed equally to this work.
§
To whom correspondence should be addressed: Mammalian Cell and
Molecular Biology Laboratory, Life Sciences Bldg. LS307, 5500 Campanile
Dr., San Diego State University, San Diego, CA 92182-4614. Tel.:
619-594-7936; Fax: 619-594-7937; E-mail: rdavis@sunstroke. sdsu.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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