Open AccessInhibition of Experimental Intimal Thickening in Mice Lacking a Novel G-Protein–Coupled Receptor
Author(s) -
Sachiyuki Tsukada,
Masaru Iwai,
Jun Nishiu,
Makoto Itoh,
Hitonobu Tomoike,
Masatsugu Horiuchi,
Yusuke Nakamura,
Toshihiro Tanaka
Publication year - 2003
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.0000043804.29963.b4
Subject(s) - medicine , restenosis , receptor , vascular smooth muscle , aorta , thickening , knockout mouse , tunica intima , pathology , anatomy , microbiology and biotechnology , cardiology , smooth muscle , biology , carotid arteries , stent , chemistry , polymer science
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 itITR (intimal thickness–related receptor). TheITR 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.