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Targeting a reduction of MCP-1 opens the door to a better understanding of the mechanistic consequences of ceramide accumulation.
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CCL2 played important roles in regulating platelet function and arterial thrombosis through the PKCalpha-P38MAPK-HSP27 pathway.
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these results suggested that the IL-1beta-induced recruitment of monocyte/macrophage lineage cells to inflamed synovial membranes in TMJ was further augmented by the cell-cell interaction-induced secretion of MCP-1 from the inflammation site, possibly resulting in prolonged inflammatory responses in TMJ synovial tissue.
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NOX4 is induced in early alcoholic liver injury and regulates CCR2/CCL2 mRNA stability thereby promoting recruitment of inflammatory cells and production of proinflammatory cytokines.
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Ccl2-Ccr2 signaling recruits a distinct fetal microchimeric population that rescues delayed maternal wound healing.
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itration reduced the potential of CCL2 to stimulate monocyte migration in diffusion gradient chemotaxis assays (p < 0.05). This was consistent with a trend towards reduced affinity of the nitrated chemokine for its cognate receptor CCR2b.
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CCL2 enables the prolonged Mesenchymal stem cells-T cell interactions needed for sufficient suppression of autoreactive T cells
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The data highlight Klf4 as an essential MCPIP1-dependent modulator of innate immunity that protects against excessive and self-destructive inflammation.
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a novel mechanism that contributes to the EMT and metastatic phenotype observed in a subset of ADT-resistant prostate cancer, where the CCL2 is stimulated through the inactivated of AR-mediated SPDEF.
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Macrophage subtypes enhanced the osteogenesis in transwell setting and the transition from M1 to M2 was associated with an increase in bone anabolic factors CCL2/MCP-1, CCL5/RANTES and IGF-1 in vitro.
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Axotomy Leads to Reduced Calcium Increase and Earlier Termination of CCL2 Release in Spinal Motoneurons.
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Our results showed that MIF regulates MCP-1 expression in hepatocytes of injured liver via CD74, CD44, and p38 MAPK in an autocrine manner.
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these studies identify a novel role for the microbiota in shaping immunity, which includes induction of CCL2 levels that control homeostatic trafficking of plasmacytoid dendritic cells
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These studies show that elevated levels of CCL2 in the CNS through increased astrocyte expression can significantly interact with the behavioral effects of alcohol.
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Topical application of glycolic acid suppresses the UVB induced IL-6, IL-8, MCP-1 and COX-2 inflammation by modulating NF-kappaB signaling pathway in mouse skin.
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Study demonstrated that CD36 deletion regulated MCP-1 expression at the transcriptional level by changing the acetylation of histones binding to the MCP-1 promoters in hepatocytes, promoting macrophage migration to the liver, and aggravating hepatic inflammatory response and fibrosis.
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Despite higher caloric intake and elevated body weights, carbohydrate restriction lowered serum MCP-1 levels, reduced prostate macrophage infiltration, reduced prostate weight, but failed to slow adenocarcinoma development.
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Data indicate that ASC-J9(R) can suppress CD4+ T cell migration via decreasing the cytokine CCL2 in vitro and in vivo.
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PDAC responds to radiotherapy by producing CCL2, which recruits Ly6C(+)CCR2(+) monocytes to support tumor proliferation and neovascularization after radiotherapy.
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Chemokine receptor 2 (CCR2(+)) monocytes invade the hippocampus between 1 and 3 d after SE. In contrast, only an occasional CD3(+) T lymphocyte was encountered 3 d after SE. The initial cellular sources of the chemokine CCL2, a ligand for CCR2, included perivascular macrophages and microglia. The induction of the proinflammatory cytokine IL-1beta was greater in FACS-isolated microglia than in brain-invading monocytes
