Könnecke, Birte

[["dc.bibliographiccitation.artnumber","e0148428"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Andresen, Lena"],["dc.contributor.author","Theodorou, Konstantina"],["dc.contributor.author","Gruenewald, Sarah"],["dc.contributor.author","Czech-Zechmeister, Bozena"],["dc.contributor.author","Koennecke, Birte"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Trendelenburg, George"],["dc.date.accessioned","2018-11-07T10:18:18Z"],["dc.date.available","2018-11-07T10:18:18Z"],["dc.date.issued","2016"],["dc.description.abstract","Toll-like receptors (TLRs) are central sensors for the inflammatory response in ischemia-reperfusion injury. We therefore investigated whether TLR4 inhibition could be used to treat stroke in a standard model of focal cerebral ischemia. Anti-TLR4/MD2-antibody (mAb clone MTS510) blocked TLR4-induced cell activation in vitro, as reported previously. Here, different routes of MTS510 application in vivo were used to study the effects on stroke outcome up to 2d after occlusion of the middle cerebral artery (MCAO) for 45min in adult male C57Bl/6 wild-type mice. Improved neurological performance, reduced infarct volumes, and reduced brain swelling showed that intravascular application of MTS510 had a protective effect in the model of 45min MCAO. Evaluation of potential long-term adverse effects of anti-TLR4-mAb-treament revealed no significant deleterious effect on infarct volumes nor neurological deficit after 14d of reperfusion in a mild model of stroke (15min MCAO). Interestingly, inhibition of TLR4 resulted in an altered adaptive immune response at 48 hours after reperfusion. We conclude that blocking TLR4 by the use of specific mAb is a promising strategy for stroke therapy. However, long-term studies with increased functional sensitivity, larger sampling sizes and use of other species are required before a clinical use could be envisaged."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.identifier.doi","10.1371/journal.pone.0148428"],["dc.identifier.isi","000369554000092"],["dc.identifier.pmid","26849209"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12842"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41412"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Evaluation of the Therapeutic Potential of Anti-TLR4-Antibody MTS510 in Experimental Stroke and Significance of Different Routes of Application"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2080"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow & Metabolism"],["dc.bibliographiccitation.lastpage","2088"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Krey, Lea"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Czech-Zechmeister, Bozena"],["dc.contributor.author","Koennecke, Birte"],["dc.contributor.author","Outeiro, Tiago Fleming"],["dc.contributor.author","Trendelenburg, George"],["dc.date.accessioned","2018-11-07T09:48:30Z"],["dc.date.available","2018-11-07T09:48:30Z"],["dc.date.issued","2015"],["dc.description.abstract","Sirtuin-2 (Sirt2) is a member of the NAD+-dependent protein deacetylase family. Various members of the sirtuin class have been found to be involved in processes related to longevity, regulation of inflammation, and neuroprotection. Induction of Sirt2 mRNA was found in the whole hemisphere after experimental stroke in a recent screening approach. Moreover, Sirt2 protein is highly expressed in myelin-rich brain regions after stroke. To examine the effects of Sirt2 on ischemic stroke, we induced transient focal cerebral ischemia in adult male Sirt2-knockout and wild-type mice. Two stroke models with different occlusion times were applied: a severe ischemia (45 minutes of middle cerebral artery occlusion (MCAO)) and a mild one (15 minutes of MCAO), which was used to focus on subcortical infarcts. Neurological deficit was determined at 48 hours after 45 minutes of MCAO, and up to 7 days after induction of 15 minutes of cerebral ischemia. In contrast to recent data on Sirt1, Sirt2(-/-) mice showed less neurological deficits in both models of experimental stroke, with the strongest manifestation after 48 hours of reperfusion. However, we did not observe a significant difference of stroke volumes or inflammatory cell count between Sirt2-deficient and wild-type mice. Thus we postulate that Sirt2 mediates myelin-dependent neuronal dysfunction during the early phase after ischemic stroke."],["dc.identifier.doi","10.1038/jcbfm.2015.178"],["dc.identifier.isi","000365891300020"],["dc.identifier.pmid","26219598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35322"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1559-7016"],["dc.relation.issn","0271-678X"],["dc.title","Knockout of silent information regulator 2 (SIRT2) preserves neurological function after experimental stroke in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]