Inhibition of experimental intimal thickening in mice lacking a novel G-protein-coupled receptor
Inhibition of experimental intimal thickening in mice lacking a novel G-protein-coupled receptor
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DOI：
10.1161/01.cir.0000043804.29963.b4
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发表时间：
2003-01-21
期刊：
影响因子：
37.8
通讯作者：
Tanaka, T
中科院分区：
文献类型：
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作者：
Tsukada, S;Iwai, M;Tanaka, T
背景-血管内膜增厚引起的再狭窄仍然是经皮腔内冠状动脉成形术（PTCA）后的主要问题。方法和结果-通过差异显示分析，我们鉴定了一个新的基因，其表达在兔主动脉导管损伤后增加。该基因主要在血管平滑肌细胞中表达，编码一种具有7个跨膜结构域的新蛋白，我们将其命名为ITR（内膜厚度相关受体）。ITR序列包含与视紫红质样GPCR（G蛋白偶联受体）超家族共有的基序。在体内分析表明，该基因的ITR蛋白的表达增加与小鼠股动脉周围的袖带放置诱导的内膜增厚。此外，ITR基因敲除小鼠被发现是耐这个实验内膜thickening.Conclusions-ITR，因此似乎是一种新的受体，可能发挥作用，在血管重塑，并可能代表一个很好的目标，为发展的药物在预防血管再狭窄。
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.