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癫痫持续状态后大鼠海马趋化因子信号的持续增加。

Prolonged increase in rat hippocampal chemokine signalling after status epilepticus.

机构信息

Dept. of Neuroscience & Pharmacology, Rudolf Magnus Institute of Neuroscience, The Netherlands.

出版信息

J Neuroimmunol. 2012 Apr;245(1-2):15-22. doi: 10.1016/j.jneuroim.2012.01.012. Epub 2012 Feb 20.

DOI:10.1016/j.jneuroim.2012.01.012
PMID:22353418
Abstract

Temporal lobe epilepsy (TLE) is one of the most common focal epilepsy syndromes. In a genome-wide expression study of the human TLE hippocampus we previously showed up-regulation of genes involved in chemokine signalling. Here we investigate in the rat pilocarpine model for TLE, whether changes in chemokine signalling occur during epileptogenesis and are persistent. Therefore we analysed hippocampal protein expression and cellular localisation of CCL2, CCL4, CCR1 and CCR5 after status epilepticus. We found increased CCL4 (but not CCL2) expression in specific populations of hilar astrocytes at 2 and 19 weeks after SE concomitant with a persistent up-regulation of its receptor CCR5. Our results show an early and persistent up-regulation of CCL4/CCR5 signalling during epileptogenesis and suggest that CCL4 signalling, rather than CCL2 signalling, could have a role in the epileptogenic process.

摘要

颞叶癫痫(TLE)是最常见的局灶性癫痫综合征之一。我们之前在一项人类 TLE 海马体的全基因组表达研究中表明,参与趋化因子信号的基因上调。在这里,我们在匹罗卡品诱导的大鼠 TLE 模型中研究了趋化因子信号是否在癫痫发生过程中发生变化并持续存在。因此,我们分析了癫痫持续状态后海马蛋白表达和趋化因子 CCL2、CCL4、CCR1 和 CCR5 的细胞定位。我们发现,癫痫持续状态后 2 周和 19 周,特定群集的海马齿状回星形胶质细胞中 CCL4(而非 CCL2)表达增加,同时其受体 CCR5 持续上调。我们的结果表明,在癫痫发生过程中,CCL4/CCR5 信号的早期和持续上调,并表明 CCL4 信号而不是 CCL2 信号可能在致痫过程中发挥作用。

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