Abstract
Platelets play a critical role in hemostasis and thrombus formation. Platelets are small, anucleate, and short-lived blood cells that are produced by the large, polyploid, and hematopoietic stem cell (HSC)-derived megakaryocytes in bone marrow. Approximately 3000 platelets are released from one megakaryocyte, and thus, it is important to understand the physiologically relevant mechanism of development of mature megakaryocytes. Many genes, including several key transcription factors, have been shown to be crucial for platelet biogenesis. Mutations in these genes can perturb megakaryopoiesis or thrombopoiesis, resulting in thrombocytopenia. Metabolic changes owing to inflammation, ageing, or diseases such as cancer, in which platelets play crucial roles in disease development, can also affect platelet biogenesis. In this review, I describe the characteristics of platelets and megakaryocytes in terms of their differentiation processes. The role of several critical transcription factors have been discussed to better understand the changes in platelet biogenesis that occur during disease or ageing.
Highlights
IntroductionAnucleate blood cells produced from mature bone marrow megakaryocytes [1]
Platelets are small, anucleate blood cells produced from mature bone marrow megakaryocytes [1]
Many studies on inherited thrombocytopenia have revealed the accumulation of megakaryocyte precursors (MkPs) and/or early MKs in the bone marrow; this indicates the developmental arrest could result in MkP hyperplasia and affect platelet biogenesis
Summary
Anucleate blood cells produced from mature bone marrow megakaryocytes [1]. Platelets are small and enucleated, they express various types of receptors, such as integrins, glycoproteins, selectins, G-protein coupled receptors (GPCRs), and receptors of the immunoglobulin type These receptors interact with their endogenous ligands, which include agonists for the initiation of hemostasis, to enforce platelet activation. On initiation of GPVI signaling after vascular injury, crosslinking of platelets with platelets and platelets with endothelial cells occur via the interaction between GPIIb/IIIa and fibrinogen, leading to thrombus formation [15,16]. Agonists such as ADP, thromboxane A2 (TxA2), and thrombin, which are secreted by activated platelets or synthesized through the coagulation cascade in the plasma membrane, are released and stimulate the platelets further via P2Y purinoceptor 12 (P2RY12), TxA2 receptor, and protease activated receptor 1 (PAR1), respectively [17,18,19] This supports platelet aggregation and thrombus formation [20].
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