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(Circulation. 2003;107:313.)
© 2003 American Heart Association, Inc.

Basic Science Reports

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; 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.

Correspondence to Yusuke Nakamura, Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, 4-6-1, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan. 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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