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首页> 外文期刊>Cytokine >Expression of cytokine genes in the aorta is altered by the deficiency in MCP-1: effect of a high-fat, high-cholesterol diet.
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Expression of cytokine genes in the aorta is altered by the deficiency in MCP-1: effect of a high-fat, high-cholesterol diet.

机译:MCP-1的缺乏会改变主动脉中细胞因子基因的表达:高脂,高胆固醇饮食的影响。

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BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) facilitates the recruitment of monocytes/macrophages into vascular intima, and it is probably involved in the regulation of other signaling pathways relevant to the pathogenesis of arteriosclerosis and metabolic disturbances. However, chemokines are redundant. Consequently, the protective effect of MCP-1 deficiency may be mediated by changes in other cytokine signals. METHODS AND RESULTS: Changes in the pattern of gene expression in the aorta were evaluated in LDLr(-/-) and MCP-1(-/-) LDLr(-/-) mice fed either chow or Western-style diet. Functional analyses were used to characterize the pathways affected and to identify biological processes in which MCP-1 may play an additional role. Some data also suggest that MCP-5 may act as a surrogate for MCP-1 deletion. Arteriosclerosis lesion and plaque composition are associated with enrichment in the cytokine-cytokine receptor interaction pathway. CONCLUSIONS: There is a complex network of interactions linking MCP-1 and other cytokines. The lack of MCP-1 limits the aortic response to atherogenic stimuli, but does not completely protect against neointima formation. Activation of alternative inflammatory pathways in the vascular wall in response to MCP-1 deficiency should be considered to fully understand the actual role of this chemokine.
机译:背景:单核细胞趋化蛋白-1(MCP-1)促进单核细胞/巨噬细胞向血管内膜的募集,并且可能参与与动脉硬化和代谢紊乱的发病机制有关的其他信号通路的调节。但是,趋化因子是多余的。因此,MCP-1缺乏的保护作用可能是由其他细胞因子信号的变化介导的。方法和结果:用低脂饮食或西式饮食的LDLr(-/-)和MCP-1(-/-)LDLr(-/-)小鼠评估了主动脉中基因表达模式的变化。功能分析被用来表征受影响的途径并鉴定MCP-1可能在其中发挥额外作用的生物学过程。一些数据还表明,MCP-5可能是MCP-1缺失的替代物。动脉硬化病变和斑块组成与细胞因子-细胞因子受体相互作用途径的富集有关。结论:有一个复杂的相互作用网络将MCP-1和其他细胞因子联系起来。 MCP-1的缺乏限制了主动脉对动脉粥样硬化刺激的反应,但不能完全防止新内膜的形成。应考虑响应MCP-1缺乏激活血管壁中的其他炎症途径,以充分了解这种趋化因子的实际作用。

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