Formation of the blood platelet
Platelets are formed during hematopoiesis via thrombopoiesis. The myeloid progenitor cells give rise to platelets in the bone marrow, which then differentiate into promegakaryocytes and megakaryocytes. The megakaryocytes remain in the bone marrow and produce proplatelets within the cytoplasm, which are released in the cytoplasmic extensions upon cytokine stimulus. The proplatelets break down into hundreds of fragments of platelets that circulate throughout the bloodstream. The nucleus of the ruptured megakaryocyte is consumed by macrophages.
The production of megakaryocytes and platelets is regulated by thrombopoietin, a hormone produced by the liver and kidneys. Thrombopoietin stimulates the development of the megakaryocytes from the myeloid progenitor cells and causes the release of the platelets. Thrombopoietin secretion is regulated by the negative feedback mechanism based on the platelet levels in the body. Old platelets are destroyed in the spleen by macrophage phagocytosis and in the liver by the Kuffer cells.
Transcription
The transcription factors and co-activators bind at the promoter of the gene proximal to the transcription start site (TSS). The recruitment of RNA polymerase II and ubiquitous transcriptional machinery factors initiate the transcription process. The sets of different TFs binding on the distal DNA elements are known as cis-regulatory modules (CRMs). The CRMs function as repressors or enhancers of gene expression via interaction with long-range DNA. The chromatin structure is further guided by epigenetic modification, which involves histone modification such as acetylation and methylation of lysine residues on H₃, and DNA methylation on cytosine; this also regulates gene expression. These processes control the accessibility of the TFs to their DNA-binding sequence and mediate the gene expression of the megakaryocyte surface receptor gene integrin alpha-2b (ITGA2B), based on the ChIP-Seq data.
Essential mediator in Atherothrombosis
The dysfunctional endothelial cells promote platelet mechanism by the two steps: Adhesion of the platelets and Aggregation of the platelets. The injury results in the accumulation of the von Willebrand factor (VWF) via endothelial cells within Weibel-Palade bodies. The disruption of endothelial cells leads to the secretion of the bodies, which involves the participation of the small G-protein Ral. The endothelial cells are released in the extracellular space as oligomers. Then, the oligomers are polymerized within the Weibel-Palade bodies of the disrupted endothelial, which anchors the circulation of the platelets. The GPIb-IX-V surface receptor on platelets mediates the adhesion of the platelets to VWF. The platelets are exposed to the microenvironment of the dysfunctional endothelial cells via the interaction between VWF/GPIb-IX-V with the platelets and collagen with GPVI and integrin α2β1. This provides the platelets with a multitude of agonists, which include collagen fibers, adenosine diphosphate, epinephrine, and thrombin. Along with this, the dysfunctional endothelial cells do not produce the platelet antagonists such as NO and prostacyclin (PGI2). The stimulation of platelets by the various agonists results in substantial changes in the structure and secretion of the granule contents of the platelet, which includes the production of the thromboxane A2 via the cyclooxygenase1-dependent mechanism and activation of the integrin αIIbβ3 (GPIIb-IIIa complex). The aggregation of the platelets promotes the formation of thrombus and exacerbates the inflammatory reaction. The platelets release the granules, provide the microenvironment with growth factors such as platelets derived growth factor (PDGF) and proinflammatory molecules such as CD40L, which contribute to the migration and the proliferation of smooth muscle cells and macrophages. The relationship between atherosclerosis and thrombosis is complex. The recruitment of inflammatory cells in the areas of the endothelial cell injury and existing plaque is the constitutive phenomenon throughout the evolution of the growth of the plaque. The platelets-leukocyte interactions represent an important pathobiological theme in atherogenesis.
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