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在没有新型G蛋白结合受体的小鼠中抑制实验性亲密厚

Shuichi Tsukada¹, Masaru Iwai, Jun Nishiu

¹Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Japan.

|January 23, 2003

概括

研究人员发现了一种新基因,ITR,与血管损伤后的内脏加厚有关. 缺乏ITR的小鼠对这种加厚有抗性,这表明ITR是预防复原的潜在药物标.

科学领域:

心血管生物学心血管生物学
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

血管缩和内脏变厚是皮肤透光冠状动脉血管形成术 (PTCA) 后的重大并发症.
识别导致内增生的分子机制对于开发有效的治疗策略至关重要.

研究的目的:

为了识别参与血管损伤后亲密厚的发展的新型基因.
在血管改造中描述已识别的基因的功能和潜在作用.

主要方法:

差异显示分析用于识别子大动脉在导管诱导损伤后表达变化的基因.
该新型基因的表达,称为ITR (极致厚度相关受体),在体内使用小鼠模型进行了分析.
产生了ITR淘汰赛小鼠,以评估它们对实验性内加厚的敏感性.

主要成果:

发现了一种新型基因ITR,在血管损伤后被发现是上调的.
ITR编码了一种具有7个跨膜域的蛋白质,属于Rhodopsin类G蛋白结合受体 (GPCR) 超级家族.
在小鼠的股骨动脉中,ITR蛋白质表达与内加厚相关,而ITR淘汰的小鼠对这一过程表现出抵抗力.

结论:

ITR是一种新型受体,涉及血管改造过程.
ITR代表了一种有前途的治疗点,用于预防血管复缩.

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