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Characterization of the Expression of Macrophage Inflammatory protein-1α (MIP-1α) and C-C Chemokine Receptor 5 (CCR5) After Kainic Acid-Induced Status Epilepticus (SE) in Juvenile Rats

Characterization of the Expression of Macrophage Inflammatory protein-1α (MIP-1α) and C-C Chemokine Receptor 5 (CCR5) After Kainic Acid-Induced Status Epilepticus (SE) in Juvenile Rats

X B Zhu, Y B Wang, O Chen, D Q Zhang, Z H Zhang, A H Cao, S Y Huang, R P Sun

Neuropathol Appl Neurobiol. 2012 Oct;38(6):602-16.

PMID: 22248156

Abstract:

Aims:
To identify the potential role of macrophage inflammatory protein-1α (MIP-1α) with its C-C chemokine receptor 5 (CCR5) in epileptogenic brain injury, we examined their expression in juvenile rat hippocampus and explored the potential link between MIP-1α, CCR5 and neuropathological alterations after status epilepticus (SE) induced by intracerebroventricular (i.c.v.) kainic acid (KA) injection.
Methods:
Based on the determination of the development of spontaneous seizures initiated by SE in developing rat brain, we firstly examined hippocampal neurone damage through Nissl and Fluoro-Jade B staining, and evaluated microglial reaction during the early phase following KA-induced SE in 21-day-old rats. MIP-1α and CCR5 protein were quantified by ELISA and Western blot respectively following mRNA by real-time PCR. We also mapped MIP-1α and CCR5 expression in the hippocampus by immunohistochemistry and identified their cellular sources using double-labelling immunofluorescence.
Results:
In juvenile rats, KA caused characteristic neurone damage in the hippocampal subfields, with accompanying microglial accumulation. In parallel with mRNA expression, MIP-1α protein in hippocampus was transiently increased after KA treatment, and peaked from 16 to 72 h. Double-labelling immunofluorescence revealed that MIP-1α was localized to microglia. Up-regulated CCR5 remained prominent at 24 and 72 h and was mainly localized to activated microglia. Further immunohistochemistry revealed that MIP-1α and CCR5 expression were closely consistent with microglial accumulation in corresponding hippocampal subfields undergoing degenerative changes.
Conclusions:
Our data indicated that MIP-1α as a regulator, linking with the CCR5 receptor, may be involved within the early stages of the epileptogenic process following SE by i.c.v. KA injection.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR4248675	MIP-1α from rat			Price

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