C-X-C Motif Chemokine Receptor 4 Blockade Promotes Tissue Repair After Myocardial Infarction by Enhancing Regulatory T Cell Mobilization and Immune-Regulatory Function.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
Napp, L Christian
Wollert, Kai C
MetadataShow full item record
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 T
AffiliationTWINCORE, Zentrum für experimentelle und klinische Infektionsforschung GmbH,Feodor-Lynen Str. 7, 30625 Hannover, Germany.
The following license files are associated with this item:
- Creative Commons
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-ShareAlike 4.0 International
- Dysfunctional and Proinflammatory Regulatory T-Lymphocytes Are Essential for Adverse Cardiac Remodeling in Ischemic Cardiomyopathy.
- Authors: Bansal SS, Ismahil MA, Goel M, Zhou G, Rokosh G, Hamid T, Prabhu SD
- Issue date: 2019 Jan 8
- Infarcted Myocardium-Primed Dendritic Cells Improve Remodeling and Cardiac Function After Myocardial Infarction by Modulating the Regulatory T Cell and Macrophage Polarization.
- Authors: Choo EH, Lee JH, Park EH, Park HE, Jung NC, Kim TH, Koh YS, Kim E, Seung KB, Park C, Hong KS, Kang K, Song JY, Seo HG, Lim DS, Chang K
- Issue date: 2017 Apr 11
- EMC10 (Endoplasmic Reticulum Membrane Protein Complex Subunit 10) Is a Bone Marrow-Derived Angiogenic Growth Factor Promoting Tissue Repair After Myocardial Infarction.
- Authors: Reboll MR, Korf-Klingebiel M, Klede S, Polten F, Brinkmann E, Reimann I, Schönfeld HJ, Bobadilla M, Faix J, Kensah G, Gruh I, Klintschar M, Gaestel M, Niessen HW, Pich A, Bauersachs J, Gogos JA, Wang Y, Wollert KC
- Issue date: 2017 Nov 7
- Interleukin-37 and Dendritic Cells Treated With Interleukin-37 Plus Troponin I Ameliorate Cardiac Remodeling After Myocardial Infarction.
- Authors: Zhu R, Sun H, Yu K, Zhong Y, Shi H, Wei Y, Su X, Xu W, Luo Q, Zhang F, Zhu Z, Meng K, Zhao X, Liu Y, Mao Y, Cheng P, Mao X, Zeng Q
- Issue date: 2016 Dec 5
- Bone marrow-derived CXCR4+ cells mobilized by macrophage colony-stimulating factor participate in the reduction of infarct area and improvement of cardiac remodeling after myocardial infarction in mice.
- Authors: Morimoto H, Takahashi M, Shiba Y, Izawa A, Ise H, Hongo M, Hatake K, Motoyoshi K, Ikeda U
- Issue date: 2007 Sep