Abstract
Platelets are abundant, small, anucleate circulating cells, serving many emerging pathophysiological roles beyond hemostasis; including active critical roles in thrombosis, injury response, and immunoregulation. In the absence of genomic DNA transcriptional regulation (no nucleus), platelets require strategic prepackaging of all the needed RNA and organelles from megakaryocytes, to sense stress (e.g., hyperglycemia), to protect themselves from stress (e.g., mitophagy), and to communicate a stress response to other cells (e.g., granule and microparticle release). Distinct from avian thrombocytes that have a nucleus, the absence of a nucleus allows the mammalian platelet to maintain its small size, permits morphological flexibility, and may improve speed and efficiency of protein expression in response to stress. In the absence of a nucleus, platelet lifespan of 7–10 days, is largely determined by the mitochondria. The packaging of 5–8 mitochondria is critical in aerobic respiration and yielding metabolic substrates needed for function and survival. Mitochondria damage or dysfunction, as observed with several disease processes, results in greatly attenuated platelet survival and increased risk for thrombovascular events. Here we provide insights into the emerging roles of platelets despite the lack of a nucleus, and the key role played by mitochondria in platelet function and survival both in health and disease.
Highlights
PLATELET DISCOVERY AND ORIGINSPlatelets are small (2–4 μm), short-lived (7–10 days), anucleate circulating cells primarily responsible for the prevention of bleeding and the maintenance of hemostasis [1, 2]
Because mitochondria play such an integral role in platelet metabolism, activation, and apoptosis, it is no surprise that mitochondrial dysfunction contribute to dysfunctional platelet activity and apoptosis in several diseases, most notably Alzheimer’s and Parkinson’s [120], cardiovascular disease (CVD) [121], diabetes mellitus [122], and sepsis [123]
While mitochondria functions are similar, its role becomes increasingly important in the nucleus-free zone of the platelet
Summary
Platelets are small (2–4 μm), short-lived (7–10 days), anucleate circulating cells primarily responsible for the prevention of bleeding and the maintenance of hemostasis [1, 2]. MKs produce billions of platelets daily through fragmentation, in which small cytoplasmic pieces bud off the megakaryocyte to become platelets [9]. MKs undergo a series of elongations to form proplatelet shafts, or cytoplasmic extensions which serve as assembly lines for platelet formation [10]. Platelets contain secretory organelles categorized as alpha, dense, and lysosomal granules, which are transported and discharged by a surface-connected open canalicular system (OCS) [13]. Platelets are released from the bone marrow into circulation, where they live for the 7–10 days [15]. Disregarded as “cellular dust” [16], platelets have only recently emerged as having more diverse homeostatic processes including wound healing, angiogenesis, immunoregulation, and inflammatory response all key components to a stress response [2, 17,18,19]
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