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Papers In Press, published online ahead of print January 22, 2001
J. Biol. Chem, 10.1074/jbc.M011655200
Submitted on December 26, 2000
Revised on January 16, 2001
Accepted on January 22, 2001
The Second Department of Internal Medicine, Ehime University School of Medicine, Onsen-gun, Ehime 791-0295
Corresponding Author: kitamiyk{at}m.ehime-u.ac.jp
CCAAT/enhancer-binding proteins (C/EBPs)-binding motifs have been identified in the promoter regions of interleukin (IL)-6, tumor necrosis factor-a and platelet-derived growth factor a receptor (PDGFaR). 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 PPARg in the regulation of IL-1b-induced PDGFaR expression in VSMCs. PPARg activators, troglitazone and 15-deoxy-D12, 14-prostaglandin J2 , inhibited IL-1b-induced PDGFaR expression, and suppressed PDGF-induced proliferation activity of VSMCs. Electromobility and supershift assay for a C/EBP motif in PDGFaR promoter region revealed that PPARg activators suppressed IL-1b-induced DNA-binding activity of C/EBPd and b. PPARg activators also suppressed IL-1b-induced C/EBPd expression. In contrast, overexpression of C/EBPd reversed the suppressive effect of PPARg activators on PDGFaR expression almost completely. From these results, we conclude that the inhibitory effect of PPARg activators on PDGFaR expression is mainly mediated by C/EBPd suppression. Regulation of C/EBPd by PPARg activators probably plays critical roles in modulating inflammatory responses in the arterial wall.
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