TLR2 has a detrimental role in mouse transient focal cerebral ischemia

Ziegler, Gina; Harhausen, Denise; Schepers, Claudia; Hoffmann, Olaf; Röhr, Christina; Prinz, Vincent; König, Janett; Lehrach, Hans; Nietfeld, Wilfried; Trendelenburg, George

doi:10.1016/j.bbrc.2007.05.157

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TLR2 has a detrimental role in mouse transient focal cerebral ischemia

Ziegler, G., Harhausen, D., Schepers, C., Hoffmann, O., Röhr, C., Prinz, V., et al. (2007). TLR2 has a detrimental role in mouse transient focal cerebral ischemia. Biochemical and Biophysical Research Communications (Orlando, FL), 359(3), 574-579. doi:10.1016/j.bbrc.2007.05.157.

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Datensatz-Permalink: https://hdl.handle.net/11858/00-001M-0000-0010-818A-D Versions-Permalink: https://hdl.handle.net/11858/00-001M-0000-0010-818B-B

Genre: Zeitschriftenartikel

Alternativer Titel : Biochem Biophys Res Commun

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Urheber:
Ziegler, Gina¹, Autor
Harhausen, Denise, Autor
Schepers, Claudia², Autor
Hoffmann, Olaf, Autor
Röhr, Christina³, Autor
Prinz, Vincent, Autor
König, Janett, Autor
Lehrach, Hans¹, Autor
Nietfeld, Wilfried¹, Autor
Trendelenburg, George, Autor

Affiliations:
1Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433550
2Max Planck Society, ou_persistent13
3Cancer Genomics (Michal-Ruth Schweiger), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1479649

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Schlagwörter: Cerebral ischemia; Toll-like receptor; TLR2; Stroke; MCAO; Knockout mice

Zusammenfassung: 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 mm3). We conclude that TLR2 up-regulation and TLR2-signaling are important events in focal cerebral ischemia and contribute to the deterioration of ischemic damage.