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Chemokine CCL2 and its receptor CCR2 are increased in the hippocampus following pilocarpine-induced status epilepticus

DOI: 10.1186/1742-2094-6-40

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Abstract:

SE was induced by pilocarpine injection. Control rats were injected with saline instead of pilocarpine. Five days after SE, CCR2 staining in neurons and glial cells was examined using imunohistochemical analyses. The number of CCR2 positive cells was determined using stereology probes in the hippocampus. CCL2 expression in the hippocampus was examined by molecular assay.Increased CCR2 was observed in the hippocampus after SE. Seizures also resulted in alterations to the cell types expressing CCR2. Increased numbers of neurons that expressed CCR2 was observed following SE. Microglial cells were more closely apposed to the CCR2-labeled cells in SE rats. In addition, rats that experienced SE exhibited CCR2-labeling in populations of hypertrophied astrocytes, especially in CA1 and dentate gyrus. These CCR2+ astroctytes were not observed in control rats. Examination of CCL2 expression showed that it was elevated in the hippocampus following SE.The data show that CCR2 and CCL2 are up-regulated in the hippocampus after pilocarpine-induced SE. Seizures also result in changes to CCR2 receptor expression in neurons and astrocytes. These changes might be involved in detrimental neuroplasticity and neuroinflammatory changes that occur following seizures.Chemokines are chemotactic cytokines that direct the migration of cells that express the appropriate chemokine receptor. Chemokine C-C motif ligand 2 (CCL2) is a potent attractant protein for monocytes, therefore being previously denominated monocyte chemoattractant protein-1 (MCP-1). The biological effects of CCL2 are mediated via interactions with its receptor, chemokine C-C motif receptor 2 (CCR2). CCR2 is a G protein-coupled receptor and has also been designated as CD192, CC-CKR-2; CKR2; CMKBR2; MCP-1-R. Upon binding to CCR2, CCL2 regulates the migration and infiltration of monocytes, T-lymphocytes and natural killer cells to regions of inflammation [1-3]. Studies using CCL2 and CCR2 knockout mice have shown that this ligand

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