CCL2 (Chemokine C-C Motif Ligand 2), also known as monocyte chemoattractant protein 1 (MCP1) or small inducible cytokine A2 (SCYA2), is a protein classified as a chemotactic cytokine or chemokine. MCP1 binds to the chemokine receptors CCR2 and CCR5. CCL2 belongs to the CC chemokine family, small soluble proteins whose main function is to regulate cell trafficking and that act as molecular signals to induce cellular migration during inflammation. Chemokines are secreted in response to signals such as proinflammatory cytokines and induce chemotaxis through the activation of G-protein-coupled receptors (GPCRs), which involves adhesion molecules and glycosaminoglycans. CCL2 is produced by a lot of cell types (endothelial, fibroblasts, epithelial, smooth muscle, monocytic, and microglial cells which are important for antiviral immune responses and in tissue), often after induction by oxidative stress, cytokines or growth factors. Unlike other chemokines such as RANTES, CCL2 exhibits a chemotactic activity only for monocytes, T-cells, basophils, NK cells and immature dendritic cells. CCL2 doesn’t attract and activate neutrophils or eosinophils. But like RANTES, CCL2 has the ability to target memory T-cells, which is not the case with other chemokines.
BACKGROUND: Chemokines are members of the chemoattractant cytokine family. They play key roles in the trafficking of leukocytes and in the induction of chemotaxis through the activation of G protein-coupled receptor. Considerable interest has been paid to these molecules to elucidate their roles in the unique inflammatory responses elicited in the central nervous system (CNS). Chemokine CCL2 (also known as monocyte chemoattractant protein-1, MCP-1) is one of the vital chemokines that control the migration and infiltration of monocytes/macrophages. CCL2 and its receptor CCR2 have been shown to be induced and involved in various neurodegenerative disorders including Alzheimer’s disease, multiple sclerosis, and ischemic brain injury. The present review will focus on the biological and pathophysiological aspects of CCL2 and CCR2 in the CNS and the possible therapeutic approaches for targeting these two proteins to combat neurodegenerative diseases.
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