Centre de Recerca Biomèdica, Hospital Universitari Sant Joan de Reus, IISPV-Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, c/Sant Joan s/n, Reus, Spain.
Cytokine. 2010 May;50(2):121-8. doi: 10.1016/j.cyto.2010.02.010. Epub 2010 Mar 5.
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.
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.
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.
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募集，它可能参与了动脉粥样硬化和代谢紊乱发病机制中其他相关信号通路的调节。然而趋化因子是冗余的。因此，MCP-1 缺乏的保护作用可能是通过其他细胞因子信号的变化来介导的。
在给予普通饮食或西式饮食的 LDLr(-/-) 和 MCP-1(-/-)LDLr(-/-) 小鼠中，评估了主动脉中基因表达模式的变化。功能分析用于表征受影响的途径，并确定 MCP-1 可能发挥额外作用的生物学过程。一些数据还表明，MCP-5 可能作为 MCP-1 缺失的替代物。动脉粥样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。
MCP-1 和其他细胞因子之间存在着复杂的相互作用网络。缺乏 MCP-1 限制了主动脉对动脉粥样硬化刺激的反应，但不能完全防止内膜形成。应该考虑到血管壁中对 MCP-1 缺乏的替代炎症途径的激活，以充分了解这种趋化因子的实际作用。
