Published Online
on December 9, 2002

A more recent version of this article appeared on January 21, 2003

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Submitted on July 2, 2002
Revised on September 6, 2002
Accepted on September 13, 2002

Inhibition of Experimental Intimal Thickening in Mice Lacking a Novel G-Protein-Coupled Receptor

Shuichi Tsukada MSc, Masaru Iwai MD, PhD, Jun Nishiu MSc, Makoto Itoh MD, PhD, Hitonobu Tomoike MD, PhD, Masatsugu Horiuchi MD, PhD, Yusuke Nakamura MD, PhD^*, and Toshihiro Tanaka MD, PhD

From the Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo (S.T., J.N., M. Itoh, Y.N., T.T.), Department of First Medical Biochemistry, Ehime University School of Medicine (M. Iwai, M.H.), and First Department of Internal Medicine, Yamagata University School of Medicine (M. Itoh, H.T.), Japan.

^* To whom correspondence should be addressed. E-mail: yusuke{at}ims.u-tokyo.ac.jp.

Background—Vascular restenosis attributable to intimal thickening remains a major problem after percutaneous transluminal coronary angioplasty (PTCA).

Methods and Results—Through differential-display analysis, we have identified a novel gene whose expression was increased after catheter injury of rabbit aorta. The gene that is expressed predominantly in vascular smooth muscle cells encodes a novel protein with 7 transmembrane domains, and we termed it ITR (intimal thickness-related receptor). The ITR sequence contains a motif common to the Rhodopsin-like GPCR (G-protein-coupled receptor) superfamily. In vivo analyses of this gene revealed that expression of ITR protein increased with intimal thickening induced by cuff placement around murine femoral artery. Furthermore, ITR-knockout mice were found to be resistant to this experimental intimal thickening.

Conclusions—ITR thus seems to be a novel receptor that may play a role in vascular remodeling and that may represent a good target for development of drugs in the prevention of vascular restenosis.

Key words: angioplasty • genes • restenosis

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