To carry out examination on the myelogram of 24 Vietnamese healthy people (12 men and 12 women) from 30 to 50 old age. The myelogram was made from 0.5ml aspirated material sucked from the right posterior iliac spine. The results showed that: - Indices of bone marrow cells on this objects were same as that using recently. However, mean number of nucleated cells in bone marrow distance (59.28(16.69G/l) and in women it is higher that that of men. Percentage and absolute number of erythrocytic line and lymphocytic line are relatively high. - Mean number of mega karyocytes per one marrow film is 13.34(6.02 in women it is also higher than that of men. This index can be useful for quantitative analysis on the mega-karyocytic line.
Megakaryocytes ; Healthy People Programs

No abstract available.
Megakaryocytes ; Plasmodium ; Plasmodium falciparum

Acquired amegakaryocytic thrombocytopenia (AAMT) is an unusual disease characterized by severe thrombocytopenia resulting from a marked decrease in bone marrow megakaryocytes. Various pathogenic mechanisms have been suggested, and several treatments have been tried, with varying outcomes. In some case reports, cyclosporine and anti-thymocyte globulin have had good clinical results in the treat of AAMT. There are few reports on the treatment of relapsed AAMT with cyclosporine. We report a patient with relapsed AAMT who was treated successfully with an additional course of cyclosporine. The initial remission was achieved with cyclosporine 4 years earlier and a second remission was induced by cyclosporine. Cyclosporine may be effective for relapsed AAMT that previously responded to cyclosporine.
Antilymphocyte Serum ; Bone Marrow ; Cyclosporine* ; Humans ; Megakaryocytes ; Thrombocytopenia*

The nuclear proto-oncogene c-myb is an essential regulator of hematopoiesis, it involves in the growth, survival, proliferation and differentiation of hematopoietic cells. More recently, different cell lines and transgenic mouse studies have suggested that c-myb plays a pivotal role in the megakaryocyte-erythroid progenitor cell lineage commitment. The deletion of the proto-oncogene c-myb would lead to profoundly impaired definitive erythropoiesis, but little influence in definitive megakaryopoiesis. Moreover, transient transfection and immunoprecipitation studies have demonstrated that c-myb exerts its physiological function in normal hematopoiesis by influencing a network of regulator molecules. Now therefore, insight into the structure, function and related molecular regulation mechanism of c-myb gene can help to further clarify its function in megakaryocyte-erythroid hematopoiesis and can provide new ideas for molecular target therapy of the platelet diseases and red blood cell diseases. In this article, c-myb structure, function and related effects involved in megakaryocyte-erythroid hematopoiesis as well as related molecular mechanisms are reviewed.
Animals ; Hematopoiesis ; Humans ; Megakaryocytes ; Mice ; Proto-Oncogene Proteins c-myb

The main physiological function of megakaryocytes is the production of platelets, whose development, maturation and platelet production are a complex regulatory process, and are involved in many factors. In recent years it was found that the lung is also the main site of megakaryocyte-producing platelets in addition to bone marrow. Based on the findings of recent years, this review summarizes the process of megakaryocyte development, maturation and platelet production, with emphasis on the analyzing the regulatory effects of apoptotic factors, miRNA, thrombopoietin and its receptors, interleukins, transcription factors and their corresponding signal pathways on platelet production. To understand the regulatory mechanism of platelet production can help to understand the pathological mechanism of platelet-related diseases and provide new ideas for the diagnosis and treatment of platelet-related diseases.
Blood Platelets ; Bone Marrow Cells ; Megakaryocytes ; Thrombopoiesis ; Thrombopoietin

Tubulin affects platelets count through the control of mitosis and the formation of pro-platelets during the maturation of megakaryoblast to platelets. Tubulin is involved in maintaining the integrity of platelet skeleton, and also participates in the change of platelet morphology during platelet activation. Some new anti-tumor drugs targeting cell mitosis are trying to reduce the effect on tubulin in order to reduce the side effect of drugs on platelet formation. In some patients with thrombocytopenia, the variation and polymorphism of the tubulin gene affect the structure of microtubule multimers, which leads to the decrease of platelet formation. This review summarized the latest progresses of tubulin in the regulation of megakaryopoiesis and thrombopoiesis.
Blood Platelets ; Humans ; Megakaryocytes ; Platelet Count ; Thrombopoiesis ; Tubulin

OBJECTIVE: To investigate the effect of enhanced autophagy in megakaryocyte to proplatelet formation in children with immune thrombocytopenia(ITP). METHODS: Giemsa staining and immunofluorescence staining were used to observe megakaryocyte morphology and proplatelet formation, Western blot was used to determine the expression of cytoskeleton protein and autophagy related protein. Autophagr regulation drugs Rap or 3-MA was used to regulate autophagy of megakaryocytes. RESULTS: Some vacuole-like structures was found in ITP megakaryocytes of the children, the expression of LC3II/I (ITP 1.32±0.18； Ctrl 0.49±0.16，P<0.05) and Atg5-Atg12 (ITP 0.69±0.17； Ctrl 0.12±0.08，P<0.05) was significantly higher in ITP children as compared with those in control group. The immu- nofluorescence staining showed that the cytoskeleton arrangement in megakaryocytes of ITP children was abnormal, and the phosphorylation of myosin light chain was also increased(ITP 0.74±0.09, Ctrl 0.05±0.02，P<0.05). In vitro, inducer or inhibitor of autophagy could regulate the production of proplatelet and the expression of cell cycle related protein, including CyclinD1（Veh 1.08±0.12; Rap 0.46±0.04; Rap+3-MA 0.70±0.03）, CyclinD2（Veh 0.47±0.04; Rap 0.27±0.04; Rap+3-MA 0.41±0.03）, P21（Veh 0.15±0.01; Rap 0.04±0.01; Rap+3-MA 0.05±0.01）. CONCLUSION Enhanced autophagy is the key factor of poor proplatelet formation in megakaryocytes of ITP children.
Autophagy ; Blood Platelets ; Humans ; Megakaryocytes ; Purpura, Thrombocytopenic, Idiopathic ; Thrombocytopenia

Objective: To observe the effect of poloxamer 188 (P188) on megakaryocyte cultivation and induction from cord blood mononuclear cells in order to obtain more megakaryocyte progenitor cells (MPC). Methods: The cord blood mononuclear cells were isolated and inoculated in cell culture bag or cell culture flask respectively. The WIGGENS shaker and cell culture bags were used to mimick WAVE Bioreactor for three-dimensional (3D) cell culture, and the P188 was added to induction medium, The cells were detected for morphology, surface marker, viability, and number on day 14. Results: In the two-dimensional (2D) culture, CD41(+), CD41(+)/CD61(+), CD61(+) megakaryocytic numbers increased significantly after adding P188 (all P<0.01). And in the 3D culture of adding P188, the cell volume became larger and the nuclear shape was irregular, the cytoplasm appeared magenta granules, and the megakaryocyte cells became more mature. By 3D culture, the expression of CD41/CD61 was (36.30±1.27)% vs (23.95±1.34)%, hence the differentiation for MPC was significantly higher than that in the 2D group (P<0.01). Furthermore, adding P188 in 3D culture resulted in highest differentiation efficiency for MPC [(59.45±1.20)%]. There were no significantly differences in terms of cell viability and cell number among 3D culture containing P188, 2D and 3D culture groups (all P>0.05). Conclusion: 3D culture was beneficial for the differentiation of MPC, but the cell viability was lower than 2D group; However, the satisfied cell growth and better induction efficiency were obtained by adding of P188, which might provide a new method of megakaryocytes production for clinical application.
Bioreactors ; Cell Differentiation ; Cells, Cultured ; Fetal Blood ; Megakaryocytes ; Poloxamer

BACKGROUND: N-myc downstream-regulated gene 2 (NDRG2), a member of a newly described family of differentiation-related genes, has been characterized as a regulator of dendritic cells. However, the role of NDRG2 on the expression and activation of transcription factors in blood cells remains poorly understood. In this study, we investigated the effects of NDRG2 overexpression on GATA-1 expression in PMA-stimulated U937 cells. METHODS: We generated NDRG2-overexpressing U937 cell line (U937-NDRG2) and treated the cells with PMA to investigate the role of NDRG2 on GATA-1 expression. RESULTS: NDRG2 overexpression in U937 cells significantly induced GATA-1 expression in response to PMA stimulation. Interestingly, JAK2/STAT and BMP-4/Smad pathways associated with the induction of GATA-1 were activated in PMA-stimulated U937-NDRG2 cells. We found that the inhibition of JAK2 activation, but not of BMP-4/Smad signaling, can elicit a decrease of PMA-induced GATA-1 expression in U937-NDRG2 cells. CONCLUSION: The results reveal that NDRG2 promotes the expression of GATA-1 through activation of the JAK2/STAT pathway, but not through the regulation of the BMP-4/Smad pathway in U937 cells. Our findings further suggest that NDRG2 may play a role as a regulator of erythrocyte and megakaryocyte differentiation during hematopoiesis.
Blood Cells ; Dendritic Cells ; Erythrocytes ; Hematopoiesis ; Humans ; Megakaryocytes ; Transcription Factors ; U937 Cells

Idiopathic thrombocytopenic purpura (ITP) is an immunologic disorder that destroys platelets and megakaryocytes. Hemorrhagic complications are common in patients with ITP. However, thrombotic complications such as coronary artery disease and cerebral infarctions are infrequent. We report a patient with ITP who developed a cerebral infarction despite thrombocytopenia after long-term danazol therapy and was negative for the antiphospholipid antibody.
Antibodies, Antiphospholipid ; Cerebral Infarction* ; Coronary Artery Disease ; Danazol ; Humans ; Megakaryocytes ; Purpura, Thrombocytopenic, Idiopathic* ; Stroke ; Thrombocytopenia