Activated platelets in emergency hematopoiesis after myocardial infarction

炎症对心肌梗死后的伤口愈合至关重要。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可促进创面愈合，减少不良心肌重构。除了从血液中局部募集外，骨髓中白细胞生成增加或髓外造血提供的白细胞与缺血后心肌炎症有重要关系。对于将白细胞需求增加的信号从损伤部位传递到骨髓造血干细胞的途径，我们知之甚少。血小板已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可增强白细胞向组织损伤部位的招募。本研究旨在探讨心肌梗死后活化血小板或其微粒在向骨髓造血干细胞远程信号传递中的作用。我们将评估活化的血小板如何与造血干细胞串扰，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可能为我们提供新的工具来监测或调节免疫反应，从而为最佳伤口愈合提供基础。

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.