Megakaryocytes, Platelets, Macrophages, and Eosinophils (Blood Cell Biochemistry)

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Cell Biol. Megakaryocytes, Platelets, Macrophages, and Eosinophils J. Robin Harris.

Blood and Bone Marrow Lab

Scianna blood group : a blood group consisting of erythrocytic antigens Sc1 formerly Sm and Sc2 formerly Bu a. Dombrock blood group [from the name of the propositus patient first observed in ] : a blood group consisting of the erythrocytic antigens Do a and Do b , most common in people of European descent. Colton blood group : a blood group consisting of erythrocytic antigens Co a , Co b. H blood group : a blood group consisting of antigen H Bombay phenotype : a rare blood phenotype produced by the interaction of genes of the ABO blood group and a rare recessive gene at a different locus, resulting in a complete lack of H antigen; cells of individuals with this phenotype lack A, B, and H antigens, and their serum contains anti-A, anti-B, and anti-H antigen.

Associated with leukocyte adhesion deficiency type 2. Gerbich blood group : a blood group consisting of the erythrocytic antigens Ge 1, Ge 2, and Ge 3 corresponding to glycophorin C and E ; although rare in most parts of the world, it has been found often in Papua New Guinea. Knops blood group : a blood group consisting of antigens Kn a , Kn b , McC a , Sl a , and Yk a , which are located on complement receptor type 1. Kamada, K.

Learning Objectives

Fujita, I. Sakurabayashi et al. Seibutsu Butsuri Kagaku 36 , pp. AMI , viral hepatitis, myoglobinuria not in myasthenia gravis and obstructive jaundice.

Megakaryocytes, Platelets, Macrophages, and Eosinophils | SpringerLink

To produce color, the reaction of the ancillary enzyme should be practiced after rising pH with alkaline solution which also stops reaction : only then PNP is convertred to quinoid. L - tartrate resistant acid phosphatase TRAP 5a and 5b isoforms. When adsorbed to platelets it is called platelet factor 1 PF1.

It is no longer considered in the scheme of hemostasis, and hence it is currently assigned neither a name nor a function. Megakaryocytes have been identified in intravascular sites within the lung, leading to a theory that platelets are formed from their parent cell predominantly in the pulmonary circulation. This mechanism requires the migration of megakaryocytes from the bone marrow into the circulation.

This may provide a simple mechanism for retaining immature megakaryocytes in the marrow and permitting mature megakaryocytes to enter the circulation, where they can liberate platelets. In addition, platelet counts are higher in the pulmonary vein than in the pulmonary artery, providing further evidence that the pulmonary bed contributes to platelet formation.

The majority of megakaryocytes were found in the right lung, suggesting filtration of megakaryocytes by the pulmonary circulation. Davis and colleagues reported that megakaryocytes and their naked nuclei were rarely observed in lung tissue even after strong stimulation of thrombopoiesis.


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In theory, pro-platelets as well as megakaryocytes may also reach the pulmonary circulation and complete their development into platelets in lung capillaries. Hartwig, in Platelets Third Edition , In theory, proplatelets as well as megakaryocytes may also reach the pulmonary circulation and complete their development into platelets in lung capillaries. Kellie R. Machlus, Joseph E. Megakaryocytes are highly specialized precursor cells that produce and release platelets into the circulation.

Understanding mechanisms by which megakaryocytes develop and give rise to platelets has fascinated hematologists for more than a century. Megakaryocytes are descended from pluripotent stem cells and undergo multiple DNA replications without cell divisions by the unique process of endomitosis. Upon completion of endomitosis, polyploid megakaryocytes begin a rapid cytoplasmic expansion phase characterized by the formation of an elaborate invaginated membrane system IMS and the accumulation of cytoplasmic proteins and granules essential for platelet function.

During the final stages of development, the megakaryocyte cytoplasm undergoes a massive reorganization into beaded cytoplasmic extensions called proplatelets. This chapter focuses on the development of megakaryocytes and evaluates the proposed mechanisms and sites of platelet formation. In addition, we review the proplatelet theory of platelet biogenesis and discuss the cytoskeletal mechanics of platelet formation.

Finally, we consider how insights gained from knockout KO animal models and human diseases have increased our understanding of megakaryocyte development and platelet formation. David J. Megakaryocytes require a large supply of energy to make platelets. This is supplied by their pool of mitochondria, which, if depleted, cause apoptosis of the megakaryocyte. When megakaryocytes are grown in tissue culture, exposure to low-level laser light LLL can enhance mitochondrial function and maintain megakaryocyte viability, and thereby increase platelet shedding in vitro.

In mice stressed with irradiation, chemotherapy, or anti-platelet antibody, brief exposure of the whole animal to LLL can prevent the thrombocytopenia that would otherwise occur. Berengere Gruson, James B. Chang et al. They noted that plasma from ITP patients with detectable antiplatelet antibodies inhibits the in vitro production and maturation of megakaryocytes, whereas plasma from control subjects or ITP patients without demonstrable antibodies did not Chang et al.

These studies would imply that the number of megakaryocytes should be reduced in these patients but instead it has been repeatedly shown that the number of megakaryocytes is usually increased.

Megakaryocytes, Platelets, Macrophages, and Eosinophils

This suggests that in vivo the megakaryocytes are made but then damaged such that they are in the marrow but relatively non-functional. T cell-mediated inhibition of megakaryocytopoiesis as well as increased apoptosis of megakaryocytes is also probably involved in the disturbance of platelet production but little studied Figure Figure Central and peripheral pathogenesis of ITP. The factors that initiate autoantibody production are unknown.

Activated antigen-presenting cells express these novel peptides on the cell surface along with costimulatory help and the relevant cytokines that facilitate the proliferation of the initiating CD4-positive T cell clones 3. Antiplatelet autoantibodies may also induce decreased megakaryocyte production and suppressed megakaryocyte maturation, which is compounded by an insufficient level of TPO 5.

Finally, cytotoxic T cells may exert cell-mediated lysis on megakaryocytes, as well as on platelets 6. Faramarz Naeim, Wayne W. Grody, in Hematopathology , Megakaryocytes may show multiple separated nuclei, hypo- or hyperlobated nuclei, vacuolated cytoplasm, and giant abnormal cytoplasmic granules.

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