TLR2 has a detrimental role in mouse transient focal cerebral ischemia

被引：232

作者：

Ziegler, Gina

Harhausen, Denise

Schepers, Claudia

Hoffmann, Olaf

Roehr, Christina

Prinz, Vincent

Koenig, Janett

Lehrach, Hans

Nietfeld, Wilfried

Trendelenburg, George

机构：

[1] Max Planck Inst Mol Genet, D-14195 Berlin, Germany

[2] Charite Univ Med Berlin, D-10098 Berlin, Germany

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2007年 / 359卷 / 03期

关键词：

cerebral ischemia; toll-like receptor; TLR2; stroke; MCAO; knockout mice;

D O I：

10.1016/j.bbrc.2007.05.157

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

A significant up-regulation of Toll-like-receptor (TLR) mRNAs between 3 and 48 h reperfusion time after induction of transient focal cerebral ischemia for 1 h was revealed by applying global gene expression profiling in postischemic mouse brains. Compared to TLR4 and TLR9, TLR2 proved to be the most significantly up-regulated TLR in the ipsilateral brain hemisphere. TLR2-protein was found to be expressed mainly in microglia in the postischemic brain tissue, but also in selected endothelial cells, neurons, and astrocytes. Additionally, TLR2-related genes with pro-inflammatory and pro-apoptotic capabilities were induced. Therefore we hypothesized that TLR2-signaling could exacerbate the primary brain damage after ischemia. Two days after induction of transient focal cerebral ischemia (1 h), we found a significant decrease of the infarct volume in TLR2 deficient mice compared to wild type mice (75 +/- 5 vs. 42 +/- 7 mm(3)). We conclude that TLR2 up-regulation and TLR2-signaling are important events in focal cerebral ischemia and contribute to the deterioration of ischemic damage. (c) 2007 Published by Elsevier Inc.

引用

页码：574 / 579

页数：6

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