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http://purl.uniprot.org/citations/19490431http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19490431http://www.w3.org/2000/01/rdf-schema#comment"

Aims

To investigate protein and gene expressions of chemokine subtypes CCR3, CCR2A and their respective ligands macrophage inflammatory protein 1-alpha (MIP-1alpha), monocyte chemotactic protein-1 (MCP-1) in the normal mouse central nervous system (CNS) and in the hippocampus at different time points during and after pilocarpine-induced status epilepticus (PISE).

Methods

CCR3 and MIP-1alpha protein expressions were mapped in the mouse CNS. The protein and gene expressions of CCR3 and CCR2A and their respective ligands MIP-1alpha, MCP-1 in the hippocampus were studies by immunocytochemical and quantitative real-time RT-PCR during and after PISE.

Results

CCR3 and MIP-1alpha gene expression and immunopositive neurones were broadly distributed in the CNS. CCR3 and CCA2A gene and their protein expression were downregulated in the hippocampus at 1 h during PISE. The protein expression of MIP-1alpha, MCP-1 decreased but gene expression increased at 2 h during PISE. In the hilus of the dentate gyrus, significant reduction of the numbers of CCR3, CCR2A, MCP-1 immunopositive neurones occurred from 1 h during to 2 months after PISE, but the number of MIP-1alpha neurones reduced from 2 h during to 2 months after PISE. Induced expression of CCR3 at 1 week, CCR2A, MCP-1 or MIP-1alpha at 1 week and 2 months after PISE was found in reactive astrocytes. MCP-1 was also demonstrated in the blood vessels of the hippocampus at 2 months after PISE.

Conclusions

CCR3 and MIP-1alpha may play important functional roles in the mouse brain. The downregulation of CCR3, CCR2A, MIP-1alpha and MCP-1 in the hippocampal neurones at the acute stage during and after PISE may weaken the neuroprotective mechanisms. However, induced expression of MCP-1 in hippocampal blood vessel may be related to changes in permeability of the blood-brain barrier during epileptogenesis."xsd:string
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http://purl.uniprot.org/citations/19490431http://purl.uniprot.org/core/author"Zhang J.T."xsd:string
http://purl.uniprot.org/citations/19490431http://purl.uniprot.org/core/author"Xu J.H."xsd:string
http://purl.uniprot.org/citations/19490431http://purl.uniprot.org/core/author"Tang Y.C."xsd:string
http://purl.uniprot.org/citations/19490431http://purl.uniprot.org/core/author"Long L."xsd:string
http://purl.uniprot.org/citations/19490431http://purl.uniprot.org/core/author"Tang F.R."xsd:string
http://purl.uniprot.org/citations/19490431http://purl.uniprot.org/core/author"Hut H.T."xsd:string
http://purl.uniprot.org/citations/19490431http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19490431http://purl.uniprot.org/core/name"Neuropathol Appl Neurobiol"xsd:string
http://purl.uniprot.org/citations/19490431http://purl.uniprot.org/core/pages"496-514"xsd:string
http://purl.uniprot.org/citations/19490431http://purl.uniprot.org/core/title"CCR3, CCR2A and macrophage inflammatory protein (MIP)-1a, monocyte chemotactic protein-1 (MCP-1) in the mouse hippocampus during and after pilocarpine-induced status epilepticus (PISE) ."xsd:string
http://purl.uniprot.org/citations/19490431http://purl.uniprot.org/core/volume"35"xsd:string
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