دورية أكاديمية
أعرض في EDS

Platelets regulate ischemia-induced revascularization and angiogenesis by secretion of growth factor-modulating factors.

التفاصيل البيبلوغرافية
العنوان: Platelets regulate ischemia-induced revascularization and angiogenesis by secretion of growth factor-modulating factors.
المؤلفون: Nording H; Cardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.; German Centre for Cardiovascular Research (DZHK), Partner Site Hamburg/Lübeck/Kiel, Lübeck, Germany., Baron L; Cardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany., Sauter M; Cardioimmunology Group, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany., Lübken A; Cardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany., Rawish E; Cardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany., Szepanowski R; Department of Neurology and Center for Translational and Behavioral Neurosciences, University Hospital Essen, Essen, Germany., von Esebeck J; Cardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany., Sun Y; Cardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany., Emami H; Cardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany., Meusel M; University Hospital, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany., Saraei R; University Hospital, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany., Schanze N; Department of Cardiology, Angiology, Haemostaseology and Medical Intensive Care, University Medical Centre Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany., Gorantla SP; Department of Hematology and Oncology, Medical Center, University of Schleswig-Holstein, Lübeck, Germany., von Bubnoff N; Department of Hematology and Oncology, Medical Center, University of Schleswig-Holstein, Lübeck, Germany., Geisler T; Department of Cardiovascular Medicine, University Hospital, Eberhard Karls University, Tuebingen, Germany., von Hundelshausen P; Institute for Cardiovascular Prevention, Ludwig Maximilians University Munich, Munich, Germany.; German Center for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany., Stellos K; German Centre for Cardiovascular Research (DZHK), Partner Site Heidelberg/Mannheim, Germany.; European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.; Department of Cardiovascular Research, European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany., Marquardt J; First Department of Medicine, University of Schleswig-Holstein, Lübeck, Germany., Sadik CD; Department of Dermatology, University of Lübeck, Lübeck, Germany., Köhl J; Institute for Systemic Inflammation Research, University of Schleswig-Holstein, Lübeck, Germany., Duerschmied D; Department of Cardiology, Angiology, Haemostaseology and Medical Intensive Care, University Medical Centre Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.; German Centre for Cardiovascular Research (DZHK), Partner Site Heidelberg/Mannheim, Germany.; European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany., Kleinschnitz C; Department of Neurology and Center for Translational and Behavioral Neurosciences, University Hospital Essen, Essen, Germany., Langer HF; Cardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.; German Centre for Cardiovascular Research (DZHK), Partner Site Hamburg/Lübeck/Kiel, Lübeck, Germany.; Cardioimmunology Group, Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany.; Department of Cardiology, Angiology, Haemostaseology and Medical Intensive Care, University Medical Centre Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.; German Centre for Cardiovascular Research (DZHK), Partner Site Heidelberg/Mannheim, Germany.; European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
المصدر: Blood advances [Blood Adv] 2023 Nov 14; Vol. 7 (21), pp. 6411-6427.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Society of Hematology Country of Publication: United States NLM ID: 101698425 Publication Model: Print Cited Medium: Internet ISSN: 2473-9537 (Electronic) Linking ISSN: 24739529 NLM ISO Abbreviation: Blood Adv Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Washington, DC : American Society of Hematology, [2016]-
مواضيع طبية MeSH: Intercellular Signaling Peptides and Proteins* , Anaphylatoxins*, Humans ; Mice ; Animals ; Ischemia/etiology ; Receptor, Anaphylatoxin C5a
مستخلص: In ischemic tissue, platelets can modulate angiogenesis. The specific factors influencing this function, however, are poorly understood. Here, we characterized the complement anaphylatoxin C5a-mediated activation of C5a receptor 1 (C5aR1) expressed on platelets as a potent regulator of ischemia-driven revascularization. We assessed the relevance of the anaphylatoxin receptor C5aR1 on platelets in patients with coronary artery disease as well as those with peripheral artery disease and used genetic mouse models to characterize its significance for ischemia and growth factor-driven revascularization. The presence of C5aR1-expressing platelets was increased in the hindlimb ischemia model. Ischemia-driven angiogenesis was significantly improved in C5aR1-/- mice but not in C5-/- mice, suggesting a specific role of C5aR1. Experiments using the supernatant of C5a-stimulated platelets suggested a paracrine mechanism of angiogenesis inhibition by platelets by means of antiangiogenic CXC chemokine ligand 4 (CXCL4, PF4). Lineage-specific C5aR1 deletion verified that the secretion of CXCL4 depends on C5aR1 ligation on platelets. Using C5aR1-/-CXCL4-/- mice, we observed no additional effect in the revascularization response, underscoring a strong dependence of CXCL4 secretion on the C5a-C5aR1-axis. We identified a novel mechanism for inhibition of neovascularization via platelet C5aR1, which was mediated by the release of antiangiogenic CXCL4.
(© 2023 by The American Society of Hematology. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution. All other rights reserved.)
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المشرفين على المادة: 0 (Intercellular Signaling Peptides and Proteins)
0 (Anaphylatoxins)
0 (Receptor, Anaphylatoxin C5a)
تواريخ الأحداث: Date Created: 20230531 Date Completed: 20231026 Latest Revision: 20231112
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC10598500
DOI: 10.1182/bloodadvances.2021006891
PMID: 37257194
قاعدة البيانات: MEDLINE
الوصف
تدمد:2473-9537
DOI:10.1182/bloodadvances.2021006891