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在CX3CR1/apolipoprotein E双淘汰赛小鼠中减少了动脉样硬化病变的形成

Christophe Combadière¹, Stéphane Potteaux, Ji-Liang Gao

¹Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Md 20892, USA.

|February 26, 2003

概括

压素 (CX3CL1) 途径对动脉样硬化发展至关重要. 在小鼠中阻断这种途径显著减少了动脉样硬化病变和巨细胞积累,表明心血管疾病的潜在治疗标.

科学领域:

心血管生物学心血管生物学
免疫学免疫学免疫学
遗传学是一个遗传学.

背景情况:

弗拉克塔尔金 (CX3CL1) 是一种在血管中发现的化学激素,通过其受体CX3CR1.1吸引白细胞.
与较低受体表达相关的CX3CR1基因变异与急性冠状动脉疾病风险降低相关.

研究的目的:

研究CX3CR1-CX3CL1通路在动脉样硬化发展中的作用.
在小鼠模型中评估CX3CR1缺乏对动脉样硬化斑块形成的影响.

主要方法:

通过基因向生成CX3CR1缺乏的小鼠 (CX3CR1(-/-)).
交叉CX3CR1(-/-) 小鼠与非脂蛋白E缺陷 (apoE(-/-)) 小鼠,以创建双重淘汰赛模型.
分析了大动脉和大动脉鼻腔中的脂质染色病变和细胞组成.

主要成果:

与对照组相比,CX3CR1/apoE双淘汰赛小鼠的胸前大动脉病变减少了59%.
大动脉鼻中的巨细胞积累在双重淘汰小鼠中减少了50%.
缺乏CX3CR1的小鼠的病变显示了斑块稳定性的特征,包括光滑肌肉细胞和原积累.

结论:

CX3CR1-CX3CL1通路在单细胞招募和动脉样硬化进展中发挥着直接而至关重要的作用.
准这种途径可能为缓解人类动脉样硬化提供治疗策略.

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