Activated platelets in emergency hematopoiesis after myocardial infarction

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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.