| Online-Ressource |
Verfasst von: | Nording, Henry Morten [VerfasserIn]  |
| Baron, Lasse [VerfasserIn]  |
| Sauter, Manuela [VerfasserIn]  |
| Lübken, Antje [VerfasserIn]  |
| Rawish, Elias [VerfasserIn]  |
| Szepanowski, Rebecca [VerfasserIn]  |
| von Esebeck, Jacob [VerfasserIn]  |
| Sun, Ying [VerfasserIn]  |
| Emami, Hossein [VerfasserIn]  |
| Meusel, Moritz [VerfasserIn]  |
| Saraei, Roza [VerfasserIn]  |
| Schanze, Nancy [VerfasserIn]  |
| Gorantla, Sivahari Prasad [VerfasserIn]  |
| von Bubnoff, Nikolas [VerfasserIn]  |
| Geisler, Tobias [VerfasserIn]  |
| von Hundelshausen, Philipp [VerfasserIn]  |
| Stellos, Konstantinos [VerfasserIn]  |
| Marquardt, Jens [VerfasserIn]  |
| Sadik, Christian D. [VerfasserIn]  |
| Köhl, Jörg [VerfasserIn]  |
| Dürschmied, Daniel [VerfasserIn]  |
| Kleinschnitz, Christoph [VerfasserIn]  |
| Langer, Harald [VerfasserIn]  |
Titel: | Platelets regulate ischemia-induced revascularization and angiogenesis by secretion of growth factor-modulating factors |
Verf.angabe: | Henry Nording, Lasse Baron, Manuela Sauter, Antje Lübken, Elias Rawish, Rebecca Szepanowski, Jacob von Esebeck, Ying Sun, Hossein Emami, Moritz Meusel, Roza Saraei, Nancy Schanze, Sivahari Prasad Gorantla, Nikolas von Bubnoff, Tobias Geisler, Philipp von Hundelshausen, Konstantinos Stellos, Jens Marquardt, Christian D. Sadik, Jörg Köhl, Daniel Duerschmied, Christoph Kleinschnitz, and Harald F. Langer |
E-Jahr: | 2023 |
Jahr: | November 14 2023 |
Umfang: | 17 S. |
Illustrationen: | Illustrationen |
Fussnoten: | Online veröffentlicht: 25 Oktober 2023 ; Gesehen am 01.10.2024 |
Titel Quelle: | Enthalten in: Blood advances |
Ort Quelle: | Washington, DC : American Society of Hematology, 2016 |
Jahr Quelle: | 2023 |
Band/Heft Quelle: | 7(2023), 21, Seite 6411-6427 |
ISSN Quelle: | 2473-9537 |
Abstract: | 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. |
DOI: | doi:10.1182/bloodadvances.2021006891 |
URL: | Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.
Volltext: https://doi.org/10.1182/bloodadvances.2021006891 |
| Volltext: https://ashpublications.org/bloodadvances/article/7/21/6411/496124/Platelets-regulate-ischemia-induced |
| DOI: https://doi.org/10.1182/bloodadvances.2021006891 |
Datenträger: | Online-Ressource |
Sprache: | eng |
K10plus-PPN: | 1903861039 |
Verknüpfungen: | → Zeitschrift |
Platelets regulate ischemia-induced revascularization and angiogenesis by secretion of growth factor-modulating factors / Nording, Henry Morten [VerfasserIn]; November 14 2023 (Online-Ressource)