PMID- 23339567 OWN - NLM STAT- MEDLINE DCOM- 20131022 LR - 20220309 IS - 1742-2094 (Electronic) IS - 1742-2094 (Linking) VI - 10 DP - 2013 Jan 22 TI - Monocyte chemoattractant protein-1 affects migration of hippocampal neural progenitors following status epilepticus in rats. PG - 11 LID - 10.1186/1742-2094-10-11 [doi] AB - BACKGROUND: Epilepsy is a common brain disorder characterized by a chronic predisposition to generate spontaneous seizures. The mechanisms for epilepsy formation remain unknown. A growing body of evidence suggests the involvement of inflammatory processes in epileptogenesis. In the present study, we investigated the involvement of monocyte chemoattractant protein-1 (MCP-1) in aberrant migration of hippocampal progenitors in rats after the insult of status epilepticus (SE). METHODS: SE was induced with pilocarpine in Sprague-Dawley rats. Transcriptional expression of MCP-1 in the dentate gyrus (DG) was measured using quantitative real-time PCR. From 1 to 28 days after SE, the temporal profiles of MCP-1 protein expression in DG were evaluated using enzyme-linked immunosorbent assay. Chemokine (C-C motif) receptor 2 (CCR2) expression in doublecortin-positive neuronal progenitors was examined using double-labeling immunohistochemistry. The involvement of MCP-1/CCR2 signaling in aberrant neuronal progenitor migration in the epileptic hippocampus was assessed in the SE rats using a CCR2 antagonist, RS102895, and the ectopic migration of neuronal progenitors was determined using Prox1/doublecortin double immunostaining. RESULTS: After SE, MCP-1 gene was significantly upregulated and its corresponding protein expression in the DG was significantly increased on days 1 and 3. Some hilar ectopic progenitor cells of SE rats expressed the MCP-1 receptor, CCR2. Notably, the ectopic migration of neuronal progenitors into hilus was attenuated by a blockade of the MCP-1/CCR2 interaction with a selective CCR2 inhibitor, RS102895. CONCLUSIONS: An increase in dentate MCP-1 is associated with seizure-induced aberrant migration of neuronal progenitors through the interaction with CCR2. The upregulation of MCP-1 after an insult of SE may play a role in the generation of epilepsy. FAU - Hung, Yu-Wen AU - Hung YW AD - Institute of Physiology, National Yang-Ming University, No,155, Sec, 2, Linong Street, Taipei, 112, Taiwan. FAU - Lai, Ming-Tsong AU - Lai MT FAU - Tseng, Yi-Jhan AU - Tseng YJ FAU - Chou, Chien-Chen AU - Chou CC FAU - Lin, Yung-Yang AU - Lin YY LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20130122 PL - England TA - J Neuroinflammation JT - Journal of neuroinflammation JID - 101222974 RN - 0 (Ccl2 protein, rat) RN - 0 (Chemokine CCL2) RN - 0 (Dcx protein, rat) RN - 0 (Doublecortin Protein) SB - IM MH - Animals MH - Cell Movement/*physiology MH - Chemokine CCL2/*biosynthesis MH - Doublecortin Protein MH - Hippocampus/*metabolism/pathology MH - Male MH - Neural Stem Cells/*metabolism/pathology MH - Rats MH - Rats, Sprague-Dawley MH - Status Epilepticus/*metabolism/pathology PMC - PMC3563591 EDAT- 2013/01/24 06:00 MHDA- 2013/10/23 06:00 PMCR- 2013/01/22 CRDT- 2013/01/24 06:00 PHST- 2012/01/19 00:00 [received] PHST- 2013/01/07 00:00 [accepted] PHST- 2013/01/24 06:00 [entrez] PHST- 2013/01/24 06:00 [pubmed] PHST- 2013/10/23 06:00 [medline] PHST- 2013/01/22 00:00 [pmc-release] AID - 1742-2094-10-11 [pii] AID - 10.1186/1742-2094-10-11 [doi] PST - epublish SO - J Neuroinflammation. 2013 Jan 22;10:11. doi: 10.1186/1742-2094-10-11.