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- W4313305881 abstract "Abstract Acute inflammatory conditions were frequently associated with increased platelet counts. However, their regulation and cellular mechanisms of acute thrombopoiesis from bone marrow megakaryocytes (MKs) were unclear. Herein, we determined the novel rupture type thrombopoiesis regulated by inflammatory cytokines, IL-1alpha, in response to acute platelet demands. The hematopoietic cytokine thrombopoietin (TPO) is believed to maintain thrombopoiesis via formation of proplatelets. However, proplatelet formation (PPF) is not the only path to platelet biogenesis. We elucidate that the IL-1alpha is a rapidly acting platelet releasing factor that induces an alternative MK rupture-type thrombopoietic pathway, characterized by cytoplasmic fragmentation with acute particle releases. During recovery after platelet depletion or under inflammatory conditions, serum IL-1alpha levels are acutely increased (within 24 h), whereas TPO is elevated only at later times (day 3 or later). In vivo, IL-1alpha administration rapidly induces rupture-type thrombopoiesis in MKs, mediating an increase in platelet counts. IL-1alpha/IL-1R1 signaling activates pERK, pAKT and caspase-3/-9, which reduces intracellular K+ concentrations, plasma membrane potential and membrane stability. Thus the balance between IL-1alpha and TPO dynamically determines MK fate, with IL-1alpha controlling rupture-type platelet release under inflammatory or acutely thrombocytopenic conditions." @default.
- W4313305881 created "2023-01-06" @default.
- W4313305881 creator A5053041377 @default.
- W4313305881 date "2015-05-01" @default.
- W4313305881 modified "2023-09-30" @default.
- W4313305881 title "Rupture-type platelet biogenesis from bone marrow megakaryocytes is regulated by IL-1alpha in response to acute inflammatory or thrombocytopenic conditions (HEM5P.236)" @default.
- W4313305881 doi "https://doi.org/10.4049/jimmunol.194.supp.120.16" @default.
- W4313305881 hasPublicationYear "2015" @default.
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