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J. Biol. Chem., Vol. 276, Issue 16, 12893-12897, April 20, 2001
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Activation
Inhibits Interleukin-1
-mediated Platelet-derived Growth Factor-
Receptor Gene Expression via CCAAT/Enhancer-binding Protein-
in
Vascular Smooth Muscle Cells*
,
From The Second Department of Internal Medicine, Ehime University
School of Medicine, Ehime 791-0295, Japan
CCAAT/enhancer-binding protein (C/EBP)-binding
motifs have been identified in the promoter regions of interleukin
(IL)-6, tumor necrosis factor-
, and platelet-derived growth
factor- receptor (PDGFR). Recently, peroxisome
proliferator-activated receptors (PPARs) have been suggested to be
important immunomodulatory mediators. Although many studies have
demonstrated that the interaction between C/EBPs and PPARs plays a
central role in lipid metabolism, expression and function of these
factors are unknown in vascular smooth muscle cells (VSMCs). In the
present study, we clarified a functional relationship between C/EBPs
and PPAR
in the regulation of IL-1
-induced PDGFR expression in
VSMCs. PPAR activators, troglitazone and
15-deoxy-
12,14-prostaglandin J2,
inhibited IL-1-induced PDGFR expression and suppressed
PDGF-induced proliferation activity of VSMCs. Electromobility shift and
supershift assays for a C/EBP motif in the PDGFR promoter region revealed that PPAR activators suppressed IL-1-induced DNA
binding activity of C/EBP
and . PPAR activators also
suppressed IL-1-induced C/EBP expression. In contrast,
overexpression of C/EBP reversed the suppressive effect of PPAR
activators on PDGFR expression almost completely. From these
results, we conclude that the inhibitory effect of PPAR activators
on PDGFR expression is mainly mediated by C/EBP suppression.
Regulation of C/EBP by PPAR activators probably plays critical
roles in modulating inflammatory responses in the arterial wall.
To whom correspondence should be addressed: The Second Department
of Internal Medicine, Ehime University School of Medicine, Ehime 791-0295, Japan. Tel.: 81-89-960-5303; Fax: 81-89-960-5306; E-mail: kitamiyk@m.ehime-u.ac.jp.
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