MCP-1/CCL2 Protein, Mouse (HEK293)

CCL2, also known as monocyte chemotactic protein 1 (MCP1), is a small cell factor belonging to the CC chemokine family. The CCL2 gene, located in the q11.2-q12 region of human chromosome 17, encodes a monomeric polypeptide with a molecular weight of 9-15 kDa, depending on the level of glycosylation. CCL2 is mainly secreted by monocytes, macrophages and dendritic cells. It is secreted by monocytes, macrophages and dendritic cells, and platelet-derived growth factor is the main inducer of the CCL2 gene. Astrocytes and microglia are also thought to be the source of CCL2^[1]. CCL2 signals through binding to and activation of CCR2 and induces a strong chemotactic response and intracellular mobilization of calcium ions. Among other things, CCL2/CCR2 can regulate cell adhesion and chemotaxis of macrophages by activating the β1 integrin and p38-MAPK signaling pathways. In addition to acting as a chemoattractant, CCL2 can also regulate brain endothelial permeability in vitro by altering tight junction (TJ) proteins and regulating the expression of endothelial adhesion molecules and leukocyte integrins as well as cytokine production. In addition, the CCL2-CCR2 signaling axis has been implicated in many inflammatory and neurodegenerative diseases, acting to recruit inflammatory cells into the CNS^[2].  Originally described as a "tumor-derived chemokine", CCL2 has been shown to be a potent chemokine for many types of immune cells and a potential target for the treatment of many diseases, such as atherosclerosis, multiple sclerosis, asthma, neuropathic pain, diabetic nephropathy, and cancer^[3].

MCP-1/CCL2 (100 ng/mL, 24 h) can induce NO production by co-treatment with IFN-γ, increases ERK phosphorylation and increases iNOS expression, suggesting that the mechanism of NO production is related to the ERK1/2 signaling pathway in peritoneal macrophages of mice, thereby increasing bacterial clearance^[3].
 CCL2 (0.05 ng/μL) promotes α-synuclein secretion and α-synuclein-induced neuronal apoptosis, and induces microglia proliferation and secretion of TNF-α, IL-1β and NO^[4].

MCP-1/CCL2 (intracerebral injection, 5-25 μg, 1 μL/h for 3 days or 0.5 μL/h for 7 days) induces FITC-albumin leakage at lower concentrations (5-20 μg) but fails or moderately induces leukocyte infiltration. Blood-brain barrier permeability and leukocyte infiltration are significantly increased at 25 μg, and extravasation is significantly enhanced in the treated CD-1 mice compared with the control group 6 h after injection. Prolonged administration for 3 or 7 days results in a significant increase in the percentage of brain water content, and decreases expression of the tight junction proteins occludin, claudin-5, ZO-1 and ZO-2^[2].