Prolonged increase in rat hippocampal chemokine signalling after status epilepticus

被引:27
作者
Kan, Anne A.
van der Hel, W. Saskia [1 ]
Kolk, Sharon M. [3 ]
Bos, Ineke W. M.
Verlinde, Suzanne A. M. W. [1 ]
van Nieuwenhuizen, Onno [2 ]
de Graan, Pierre N. E.
机构
[1] Univ Med Ctr Utrecht, Div Surg Specialties, Dept Anat, Utrecht, Netherlands
[2] Univ Med Ctr Utrecht, Dept Child Neurol, Utrecht, Netherlands
[3] Radboud Univ Nijmegen, Fac Sci, Ctr Neurosci, Dept Mol Anim Physiol,Donders Inst Brain Cognit &, NL-6525 ED Nijmegen, Netherlands
关键词
Temporal lobe epilepsy; Epileptogenesis; Chemokines; CCL4; CCRS; TEMPORAL-LOBE EPILEPSY; BLOOD-BRAIN-BARRIER; MONOCYTE CHEMOATTRACTANT PROTEIN-1; CENTRAL-NERVOUS-SYSTEM; ANTIEPILEPTIC DRUGS; STIMULATES EXPRESSION; MESSENGER-RNA; RECEPTOR CCR5; NEURON LOSS; INFLAMMATION;
D O I
10.1016/j.jneuroim.2012.01.012
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:15 / 22
页数:8
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