Activated platelets in emergency hematopoiesis after myocardial infarction

炎症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，协调着坏死的清除和组织重塑的调节。心肌梗死后炎症反应的特异性调节可促进创面愈合，减少不利的心肌重构。除了从血液中局部募集外，通过增加骨髓中白细胞的产生或通过髓外造血来提供白细胞与缺血后心肌炎症密切相关。从损伤部位到骨髓中的造血干细胞，携带白细胞需求增加的信号的通路知之甚少。人们认识到，血小板具有免疫调节功能，增加了血小板活化的重要性，使其超越聚集和参与心肌梗死后的止血。已知的是，血小板与白细胞的串扰可以促进白细胞在组织损伤部位的募集。本研究旨在探讨活化的血小板或其微粒在心肌梗死后向骨髓中的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。深入了解心肌梗死后的炎症途径和信号转导可能为我们监测或调节免疫反应提供新的工具，从而为创面的最佳愈合提供依据。

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.