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Originally published In Press as doi:10.1074/jbc.M104560200 on January 2, 2002

J. Biol. Chem., Vol. 277, Issue 12, 9676-9683, March 22, 2002
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Transcription Suppression of Thromboxane Receptor Gene by Peroxisome Proliferator-activated Receptor-gamma via an Interaction with Sp1 in Vascular Smooth Muscle Cells*

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

From the Division of Nephrology, Endocrinology, and Vascular Medicine, Department of Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo-cho, Aoba-ku, Sendai 980-8574, Japan

Thromboxane (TX) A2 exerts contraction and proliferation of vascular smooth muscle cells (VSMCs) via its specific membrane TX receptor (TXR), possibly leading to the progression of atherosclerosis. A nuclear hormone receptor, peroxisome proliferator-activated receptor (PPAR)-gamma , has recently been reported to be expressed in VSMCs. Here we examined a role of PPAR-gamma in TXR gene expression in VSMCs. PPAR-gamma ligands 15-deoxy-Delta 12,14-prostaglandin J2 and troglitazone reduced TXR mRNA expression levels as well as cell growth as assessed by [3H]thymidine incorporation. Transcriptional activity of the TXR gene promoter was suppressed with PPAR-gamma ligands, and the suppression was augmented further by PPAR-gamma overexpression. By deletion and mutation analyses, the transcription suppression was shown to be the result of a -22/-7 GC box-related sequence (upstream of transcription start site). Electrophoretic mobility shift assays also showed that the sequence was bound by Sp1 but not by PPAR-gamma , and the formation of a Sp1·DNA complex was inhibited either by coincubation with PPAR-gamma or PPAR-gamma ligand 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 antiatherosclerotic action by inhibiting TXR gene expression in VSMCs.

* This work was supported in part by Grants-in-aid 09671018 and 09470236 from the Ministry of Education, Science, and Culture of Japan, the Kanae Foundation for Life and Socio-Medical Science, the Mochida Memorial Foundation for Medical and Pharmaceutical Research, the Takeda Metabolic Disorder Research Foundation, and Sankyo Co. Ltd., Japan.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.

Dagger To whom correspondence should be addressed. Tel.: 81-22-717-7163; Fax: 81-22-717-7168; E-mail: akiras2i@mail.cc.tohoku.ac.jp.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.


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