Activated platelets in emergency hematopoiesis after myocardial infarction

活化血小板在心肌梗死后紧急造血中的作用

• 批准号: 311869289
• 负责人: Privatdozent Dr. Timo Sebastian Heidt
• 金额: --
• 依托单位: Klinik für Kardiologie und Angiologie
• 依托单位国家: 德国
• 项目类别: Research Grants
• 财政年份: 2016
• 资助国家: 德国
• 起止时间: 2015-12-31 至 2020-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/311869289?language=en
• 关键词: Activated; platelets; emergency; hematopoiesis; after

Inflammation is essential for wound healing after myocardial infarction. Leukocytes, especially neutrophils, monocytes and macrophages, orchestrate removal of necrosis and regulation of tissue remodeling. Specific modulation of post-infarct inflammation could improve wound healing and reduce adverse myocardial remodeling. Next to local recruitment from the blood, leukocyte supply via increased leukocyte production in the bone marrow or by extramedullary hematopoiesis, is of mayor relevance for post-ischemic myocardial inflammation. Little is known about the pathways that carry the signals for increased demand of leukocytes from the site of injury to hematopoietic stem cells in the bone marrow. Platelets have been appreciated to harbor immunoregulatory functions increasing the significance of platelet activation beyond aggregation and participation in hemostasis after myocardial infarction. Platelet crosstalk to leukocytes is known to enhance recruitment of leukocytes to the site of tissue injury. This study aims to investigate the role of activated platelets or their microparticles in remote signaling to hematopoietic stem cells in the bone marrow after myocardial infarction. We will assess how activated platelets may crosstalk to hematopoietic stem cells and how this can impact on myocardial inflammation and wound healing. Thorough understanding of inflammatory pathways and signaling after myocardial infarction may provide us with new tools to monitor or modulate the immune response in order to provide the basis for optimal wound healing.

炎症反应是心肌梗死后伤口愈合所必需的。白细胞，特别是中性粒细胞、单核细胞和巨噬细胞，协调坏死的清除和组织重塑的调节。特异性调节梗死后炎症反应可促进创伤愈合，减少不良心肌重塑。除了从血液中局部募集外，通过骨髓中白细胞生成增加或髓外造血作用提供的白细胞供应与缺血后心肌炎症关系最大。很少有人知道的途径，携带的信号，增加需求的白细胞从损伤部位的造血干细胞在骨髓中。 血小板被认为具有免疫调节功能，增加了血小板活化的重要性，而不仅仅是聚集和参与心肌梗死后的止血。已知血小板对白细胞的串扰增强白细胞向组织损伤部位的募集。本研究旨在探讨活化血小板及其微粒在心肌梗死后向骨髓造血干细胞发出远程信号中的作用。我们将评估活化的血小板如何与造血干细胞相互作用，以及这如何影响心肌炎症和伤口愈合。 彻底了解心肌梗死后的炎症通路和信号传导可能为我们提供新的工具来监测或调节免疫反应，以便为最佳伤口愈合提供基础。

项目成果

P2Y12-dependent regulation of emergency hematopoiesis after myocardial infarction

心肌梗死后紧急造血的 P2Y12 依赖性调节

• DOI: 10.1093/ehjci/ehaa946.3730
• 发表时间: 2020
• 期刊: European Heart Journal
• 影响因子: 39.3
• 作者: H Seung;C Wadle;T Hopp;D Duerschmied;I Hilgendorf;D Wolf;P Stachon;C Bode;C Von Zur Muehlen;T Heidt
• 通讯作者: T Heidt

P3443P2Y12 is involved in emergency hematopoiesis after myocardial infarction

P3443P2Y12参与心肌梗死后紧急造血

• DOI: 10.1093/eurheartj/ehy563.p3443
• 发表时间: 2018
• 期刊: European Heart Journal
• 影响因子: 39.3
• 作者: H Seung;C Wadle;T Hopp;D Duerschmied;I Hilgendorf;D Wolf;P Stachon;C Bode;C Von Zur Muehlen;T Heidt
• 通讯作者: T Heidt