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A more recent version of this article appeared on March 15, 2002
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M104560200v1
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Papers In Press, published online ahead of print January 2, 2002
J. Biol. Chem, 10.1074/jbc.M104560200
Submitted on May 18, 2001
Revised on December 18, 2001
Accepted on December 31, 2001

Transcription suppression of thromboxane receptor gene by peroxisome proliferator-activated receptor-gamma via an interaction with Sp1 in vascular smooth muscle cells

Akira Sugawara, Akira Uruno, Masataka Kudo, Yukio Ikeda, Kazunori Sato, Yoshihiro Taniyama, Sadayoshi Ito, and Kazuhisa Takeuchi

Medicine, Tohoku University Graduate School of Medicine, Sendai, Miyagi 980-8574

Corresponding Author: akiras2i{at}mail.cc.tohoku.ac.jp

Thromboxane (TX) A2 exerts contraction and proliferation of vascular smooth muscle cells (VSMCs) via its specific membrane TX receptor (TXR), possibly leading to progression of atherosclerosis. A nuclear hormone receptor, peroxisome proliferator-activated receptor (PPAR)-gamma has recently been reported to be expressed in VSMCs. We here examined a role of PPAR-gamma in TXR gene expression in VSMCs. PPAR-gamma ligands 15-deoxy-delta12,14-prostaglandin J2 and troglitazone reduced TXR mRNA expression levels as well as the cell growth assessed by 3H-thymidine incorporation. Transcription activity of TXR gene promoter was suppressed with PPAR-gamma ligands, and the suppression was further augmented by PPAR-gamma overexpression. By deletion and mutation analyses, the transcription suppression was shown to be due to the -22/-7 GC-box related sequence. Electrophoretic mobility shift assays also showed that the sequence was bound by Sp1 but not by PPAR-gamma, and the formation of Sp1-DNA complex was inhibited either by co-incubation with PPAR-gamma or PPAR-gamma ligands treatment of VSMCs. Moreover, glutathione S-transferase pull-down assays demonstrated a direct interaction between PPAR-gamma and Sp1. In conclusion, PPAR-gamma suppresses TXR gene transcription via an interaction with Sp1. PPAR-gamma may possibly have an anti-atherosclerotic action by inhibiting TXR gene expression in VSMCs.


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