What is platelet ?
Platelets are the smallest of the many types of cells in circulating blood, averaging only 2.0 to 5.0 μm in diameter, 0.5 μm in thickness, and having a mean cell volume of 6 to 10 femtoliters. Inconsequential size does not bother the platelet. It prefers to remain obscure throughout its 7- to 10-day life span. If it can reach its final destination in the reticuloendothelial system without having exercised a function in hemostasis or been involved in thrombotic events, its life would be considered a complete success. Yet, the life of the host in whom the platelet resides is not easy. Sooner or later, a generation of platelets will be called upon to exercise functions useful or essential for host survival. Unfortunately, platelet function important to host preservation may also contribute to host destruction. Thus, it is important to understand platelet structure, biochemistry, physiology, and pathology to foster normal function and block involvement in occlusive vascular and thrombotic disease. The purpose
of this article is to contribute to these objectives by presenting current knowledge of platelet structure and structural physiology. Occasionally, examples of abnormal platelet structure will be included to assist in the understanding of normal platelet morphology and function.
The Peripheral Zone
a. General Features
The platelet plasma membrane is relatively smooth compared with that of leukocytes in circulating blood, but low-voltage, high-resolution scanning electron microscopy suggested it has a fi ne, rugose appearance, resembling the gyri and sulci on the surface of the brain
The tiny folds may provide additional membrane needed when platelets spread on surfaces. Small openings of the surface
connected open canalicular system (SCCS) are randomly dispersed on the otherwise featureless platelet exterior
glycocalyx rests is a typical unit membrane and does not differ in appearance from the membrane covering other cells. Yet, it serves an extremely important role in the acceleration of clotting ,
Platelet Formation
A. Mechanisms of Platelet Production
Although it has been universally accepted that platelets derive from megakaryocytes, the mechanisms by which platelets form and release from these precursor cells remain controversial. Throughout the years, several models of platelet production have been proposed. These include (a) platelet budding, (b) cytoplasmic fragmentation via the DMS, and (c) proplatelet formation. Past studies attempting
to discriminate between these mechanisms of platelet bio-genesis have been hampered by the requirement of sampling bone marrow to obtain megakaryocytes, the relative infrequency of megakaryocytes in the marrow, and the lack of in vitro systems that faithfully reconstitute platelet formation. However, the discovery of thrombopoietin (TPO), a cytokine that binds to the megakaryocyte-specifi c receptor c-MPL and promotes the growth and development of mega-
karyocyte precursors, has led to the emergence of culture systems that recapitulate platelet biogenesis and resulted in a new understanding of the terminal differentiation phase of thrombopoiesis. Several models of platelet biogenesis are discussed next.
1. Budding from the Megakaryocyte Surface.
Based on scanning electron micrographs of megakaryocytes with apparent platelet-size blebs on their surface, it was proposed that platelets shed from the periphery of the megakaryocyte cytoplasm. Examination of these structures by thin section electron microscopy, however, revealed that these blebs did not contain platelet organelles, an observation inconsistent with the concept of platelet budding as a mechanism for platelet release. In addition, the platelet buds were probably confused with the pseudopods that extend from mature megakaryocytes during the initial stages of proplate let formation.
2. Cytoplasmic Fragmentation via the Demarcation Membrane System.
The DMS, described in detail by Yamada in 1957, has been proposed to defi ne preformed
“platelet territories” within the cytoplasm of the megakaryo cyte. Microscopists recognized that maturing megakaryocytes became fi lled with membranes and platelet-specific organelles, and postulated that these membranes formed a system that defi ned territories or fi elds for developing platelets. Release of individual platelets was proposed to occur by a massive fragmentation of the megakaryocyte cytoplasm along DMS fracture lines residing between these fields. The DMS model predicts that platelets form through an extensive internal membrane reorganization process.
Tubular membranes, which may originate from invagination of the megakaryocyte plasma membrane, are predicted to interconnect and branch, forming a continuous network throughout the cytoplasm. The fusion of adjacent tubules has been proposed as a mechanism to generate a fl at membrane that ultimately surrounds the cytoplasm of a putative platelet. Models attempting to use the DMS to explain how the megakaryocyte cytoplasm becomes subdivided into platelet volumes and enveloped by its own membrane have lost support because of several inconsistent observations. For example, if platelets are delineated within the megakaryocyte cytoplasm by the DMS, then platelet fields should
exhibit structural characteristics of platelets, which is not the case. Platelet territories within the megakaryocyte cytoplasm lack marginal microtubule coils, the most characteristic feature of resting platelet structure. In addition, there are no studies directly demonstrating that platelet fields shatter into mature, functional platelets. In contrast, studies that focused on the DMS of
megakaryocytes before and after proplatelet retraction induced by microtubule depolymerizing agents suggest this specialized membrane system may function primarily as a membrane reservoir that evaginates to provide plasma membrane for the growth of proplatelets. Radley and Haller
considered the name DMS to be a misnomer, and suggested invagination membrane system as a more suitable name to describe this membranous network.
3. Proplatelet Formation
a. The Proplatelet Theory. The term proplatelet is generally used to describe long (up to millimeters in length), thin cytoplasmic processes emanating from megakaryocytes. These extensions are typically characterized by multiple platelet-size swellings linked together by thin cytoplasmic bridges and are
concept of platelets arising from these pseudopodialike structures dates originally to 1906, when Wright recognized that platelets originate from megakaryocytes and described “the detachment of plate-like fragments or segments from pseudopods” of megakaryocytes. Thiery and Bessis, and Behnke, later described in more detail the structure of these cytoplasmic processes extending from megakaryocytes during platelet formation. The classic “pro-platelet theory” was introduced by Becker and DeBruyn, who proposed that megakaryocytes form long pseudopod-like processes that subsequently fragment to generate individual platelets. In this early model, the DMS was still proposed to subdivide the megakaryocyte cytoplasm into platelet areas. Radley and Haller later developed the “flow model,” which postulated that platelets derived exclusively from the interconnected platelet-size beads connected along the shaft of proplatelets, and suggested that the DMS did not function to defi ne platelet fi elds, but as a reservoir of surface membrane to be evaginated during proplatelet formation. Developing platelets were assumed to become encased by plasma membrane only as proplatelets were formed.
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