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dc.contributor.authorWang, Yong
dc.contributor.authorDembowsky, Klaus
dc.contributor.authorChevalier, Eric
dc.contributor.authorStüve, Philipp
dc.contributor.authorKorf-Klingebiel, Mortimer
dc.contributor.authorLochner, Matthias
dc.contributor.authorNapp, L Christian
dc.contributor.authorFrank, Heike
dc.contributor.authorBrinkmann, Eva
dc.contributor.authorKanwischer, Anna
dc.contributor.authorBauersachs, Johann
dc.contributor.authorGyongyosi, Mariann
dc.contributor.authorSparwasser, Tim
dc.contributor.authorWollert, Kai C
dc.date.accessioned2019-02-06T14:38:18Z
dc.date.available2019-02-06T14:38:18Z
dc.date.issued2019-01-30
dc.identifier.issn1524-4539
dc.identifier.pmid30696265
dc.identifier.doi10.1161/CIRCULATIONAHA.118.036053
dc.identifier.urihttp://hdl.handle.net/10033/621682
dc.description.abstractAcute myocardial infarction (MI) elicits an inflammatory response that drives tissue repair and adverse cardiac remodeling. Inflammatory cell trafficking after MI is controlled by C X-C motif chemokine ligand 12 (CXCL12) and its receptor, C-X-C motif chemokine receptor 4 (CXCR4). CXCR4 antagonists mobilize inflammatory cells and promote infarct repair, but the cellular mechanisms are unclear. We investigated the therapeutic potential and mode of action of the peptidic macrocycle CXCR4 antagonist POL5551 in mice with reperfused MI. We applied cell depletion and adoptive transfer strategies using lymphocyte-deficient Rag1 knockout mice; DEREG mice, which express a diphtheria toxin receptor-enhanced green fluorescent protein fusion protein under the control of the promoter/enhancer region of the regulatory T (T Intraperitoneal POL5551 injections in wild-type mice (8 mg/kg at 2, 4, 6, and 8 d) enhanced angiogenesis in the infarct border-zone, reduced scar size, and attenuated left ventricular remodeling and contractile dysfunction at 28 d. Treatment effects were absent in splenectomized wild-type mice, Rag1 knockout mice, and T Our data confirm CXCR4 blockade as a promising treatment strategy after MI. We identify dendritic cell-primed splenic Ten_US
dc.language.isoenen_US
dc.publisherLippinscott, Williams & Wilkins; American Heart Associationen_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectCXCR4 antagonisten_US
dc.subjectRegulatory T cellsen_US
dc.titleC-X-C Motif Chemokine Receptor 4 Blockade Promotes Tissue Repair After Myocardial Infarction by Enhancing Regulatory T Cell Mobilization and Immune-Regulatory Function.en_US
dc.typeArticleen_US
dc.contributor.departmentTWINCORE, Zentrum für experimentelle und klinische Infektionsforschung GmbH,Feodor-Lynen Str. 7, 30625 Hannover, Germany.en_US
refterms.dateFOA2019-02-06T14:38:19Z
dc.source.journaltitleCirculation


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