Relevant bibliographies by topics / Thrombopoiesis

Academic literature on the topic 'Thrombopoiesis'

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Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Thrombopoiesis"

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Kaushansky, Kenneth. "Historical review: megakaryopoiesis and thrombopoiesis." Blood 111, no. 3 (February 1, 2008): 981–86. http://dx.doi.org/10.1182/blood-2007-05-088500.

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Abstract The study of thrombopoiesis has evolved greatly since an era when platelets were termed “the dust of the blood,” only about 100 years ago. During this time megakaryocytes were identified as the origin of blood platelets; marrow-derived megakaryocytic progenitor cells were functionally defined and then purified; and the primary regulator of the process, thrombopoietin, was cloned and characterized and therapeutic thrombopoietic agents developed. During this journey we continue to learn that the physiologic mechanisms that drive proplatelet formation can be recapitulated in cell-free systems and their biochemistry evaluated; the molecular underpinnings of endomitosis are being increasingly understood; the intracellular signals sent by engagement of a large number of megakaryocyte surface receptors have been defined; and many of the transcription factors that drive megakaryocytic fate determination have been identified and experimentally manipulated. While some of these biologic processes mimic those seen in other cell types, megakaryocytes and platelets possess enough unique developmental features that we are virtually assured that continued study of thrombopoiesis will yield innumerable clinical and scientific insights for many decades to come.
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Kaushansky, K. "Thrombopoietin: a tool for understanding thrombopoiesis." Journal of Thrombosis and Haemostasis 1, no. 7 (July 2003): 1587–92. http://dx.doi.org/10.1046/j.1538-7836.2003.00273.x.

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Kuter, D. J. "Thrombopoietins and Thrombopoiesis: A Clinical Perspective." Vox Sanguinis 74, S2 (June 1998): 75–85. http://dx.doi.org/10.1111/j.1423-0410.1998.tb05400.x.

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Kaushansky, Kenneth. "Determinants of platelet number and regulation of thrombopoiesis." Hematology 2009, no. 1 (January 1, 2009): 147–52. http://dx.doi.org/10.1182/asheducation-2009.1.147.

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Abstract Our understanding of thrombopoiesis has improved greatly in the last two decades with the availability of in vitro assays of megakaryocyte progenitor cell growth, with the cloning and characterization of stem cell factor (SCF) and thrombopoietin (Tpo), the latter the primary humoral regulator of this process, and with the generation of genetically altered murine models of thrombopoietic failure and excess. While SCF affects developmentally early aspects of megakaryocyte growth, Tpo affects nearly all aspects of platelet production, from hematopoietic stem cell (HSC) self-renewal and expansion, through stimulation of megakaryocyte progenitor cell proliferation, to supporting their maturation into platelet-producing cells. The molecular and cellular mechanisms through which the marrow microenvironment and humoral mediators affect platelet production provide new insights into the interplay between intrinsic and extrinsic influences on hematopoiesis, and highlight new opportunities to translate basic biology into clinical advances.
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McCormack, Matthew P., Mark A. Hall, Simone M. Schoenwaelder, Quan Zhao, Sarah Ellis, Julia A. Prentice, Ashleigh J. Clarke, et al. "A critical role for the transcription factor Scl in platelet production during stress thrombopoiesis." Blood 108, no. 7 (October 1, 2006): 2248–56. http://dx.doi.org/10.1182/blood-2006-02-002188.

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Abstract The generation of platelets from megakaryocytes in the steady state is regulated by a variety of cytokines and transcription factors, including thrombopoietin (TPO), GATA-1, and NF-E2. Less is known about platelet production in the setting of stress thrombopoiesis, a pivotal event in the context of cytotoxic chemotherapy. Here we show in mice that the transcription factor Scl is critical for platelet production after chemotherapy and in thrombopoiesis induced by administration of TPO. Megakaryocytes from these mice showed appropriate increases in number and ploidy but failed to shed platelets. Ultrastructural examination of Scl-null megakaryocytes revealed a disorganized demarcation membrane and reduction in platelet granules. Quantitative real-time polymerase chain reaction showed that Scl-null platelets lacked NF-E2, and chromatin immunoprecipitation analysis demonstrated Scl binding to the NF-E2 promoter in the human megakaryoblastic-cell line Meg-01, along with its binding partners E47, Lmo2, and the cofactors Ldb1 and GATA-2. These findings suggest that Scl acts up-stream of NF-E2 expression to control megakaryocyte development and platelet release in settings of thrombopoietic stress.
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Pick, Marjorie, Chava Perry, Tsvee Lapidot, Cinthya Guimaraes-Sternberg, Elizabeth Naparstek, Varda Deutsch, and Hermona Soreq. "Stress-induced cholinergic signaling promotes inflammation-associated thrombopoiesis." Blood 107, no. 8 (April 15, 2006): 3397–406. http://dx.doi.org/10.1182/blood-2005-08-3240.

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AbstractTo study the role of the stress-induced “readthrough” acetylcholinesterase splice variant, AChE-R, in thrombopoiesis, we used transgenic mice overexpressing human AChE-R (TgR). Increased AChE hydrolytic activity in the peripheral blood of TgR mice was associated with increased thrombopoietin levels and platelet counts. Bone marrow (BM) progenitor cells from TgR mice presented an elevated capacity to produce mixed (GEMM) and megakaryocyte (Mk) colonies, which showed intensified labeling of AChE-R and its interacting proteins RACK1 and PKC. When injected with bacterial lipopolysaccharide (LPS), parent strain FVB/N mice, but not TgR mice, showed reduced platelet counts. Therefore, we primed human CD34+ cells with the synthetic ARP26 peptide, derived from the cleavable C-terminus of AChE-R prior to transplantation, into sublethally irradiated NOD/SCID mice. Engraftment of human cells (both CD45+ and CD41+ Mk) was significantly increased in mice that received ARP26-primed CD34+ human cells versus mice that received fresh nonprimed CD34+ human cells. Moreover, ARP26 induced polyploidization and proplatelet shedding in human MEG-01 promegakaryotic cells, and human platelet engraftment increased following ex vivo expansion of ARP26-treated CD34+ cells as compared to cells expanded with thrombopoietin and stem cell factor. Our findings implicate AChE-R in thrombopoietic recovery, suggesting new therapeutic modalities for supporting platelet production.
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Kaushansky, Kenneth. "Thrombopoiesis." Seminars in Hematology 52, no. 1 (January 2015): 4–11. http://dx.doi.org/10.1053/j.seminhematol.2014.10.003.

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Miyakawa, Y., A. Oda, BJ Druker, H. Miyazaki, M. Handa, H. Ohashi, and Y. Ikeda. "Thrombopoietin induces tyrosine phosphorylation of Stat3 and Stat5 in human blood platelets." Blood 87, no. 2 (January 15, 1996): 439–46. http://dx.doi.org/10.1182/blood.v87.2.439.bloodjournal872439.

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Thrombopoietin is known to be essential for megakaryocytopoiesis and thrombopoiesis. Recently, we and others have shown that thrombopoietin induces rapid tyrosine phosphorylation of Jak2 and other proteins in human platelets and BaF3 cells, genetically engineered to express c- Mpl, a receptor for thrombopoietin. The Jak family of tyrosine kinases are known to mediate some of the effects of cytokines or hematopoietic growth factors by recruitment and tyrosine phosphorylation of a variety of Stat (signal transducers and activators of transcription) proteins. Hence, we have investigated whether Stat proteins are present in platelets and, if so, whether they become tyrosine phosphorylated in response to thrombopoietin. We immunologically identified Stat1, Stat2, Stat3, and Stat5 in human platelet lysates. Thrombopoietin induced tyrosine phosphorylation of Stat3 and Stat5 in these cells. Thrombopoietin also induced tyrosine phosphorylation of Stat3 and Stat5 in FDCP-2 cells genetically engineered to constitutively express human c-Mpl. Thus, our data indicate that Stat3 and Stat5 may be involved in signal transduction after ligand binding to c-Mpl and that this event may have a role in megakaryopoiesis/thrombopoiesis or possibly a mature platelet function such as aggregation.
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Radley, JM, and SL Ellis. "Ineffective Thrombopoiesis." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (August 12, 1990): 266–67. http://dx.doi.org/10.1017/s0424820100158881.

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In effective thrombopoies is has been inferred to occur in several disease sates from considerations of megakaryocyte mass and platelet kinetics. Microscopic examination has demonstrated increased numbers of megakaryocytes, with a typical forms particularly pronounced, in primary myelofibrosis. It has not been documented if megakaryocyte ever fail to reach maturity in non-pathological situations. A major difficulty of establishing this is that the number of megakaryocytes normally present in the marrow is extremely low. A large transient increase in megakaryocytopoiesis can how ever be induced in mice by an injection of 5-fluorouracil. We have utilised this treatment and report here evidence for in effective thrombopoies is in healthy mice.Adult mice were perfused (2% glutaraldehyde in 0.08M phosphate buffer, pH 7.4) 8 days following an injection of 5-fluorouracil (150mg/kg). Femurs were subsequently decalcified in 10% neutral E.D.T.A. and embedded in Spurrs resin. Transverse sections of marrow revealed many megakaryocytes at various stages of maturity. Occasional megakaryocytes (less than 1%) were found to be under going degeneration prior to achieving full maturation and releasing cytoplasm as platelets. These cells were characterized by a peripheral rim of dense cytoplasm which enveloped a mass of organelles and vacuoles (Fig. 1). Numerous microtubules were foundaround and with in the organelle-rich zone (Fig 2).
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Jilma-Stohlawetz, P., M. Homoncik, B. Jilma, C. C. Folman, A. E. G. KR Von Dem Borne, G. Bernaschek, J. Deutinger, B. Ulm, W. Eppel, and S. Panzer. "High levels of reticulated platelets and thrombopoietin characterize fetal thrombopoiesis." British Journal of Haematology 112, no. 2 (February 2001): 466–68. http://dx.doi.org/10.1046/j.1365-2141.2001.02524.x.

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Dissertations / Theses on the topic "Thrombopoiesis"

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Sundaramoorthi, Hemalatha. "Identification of Hox Genes Controlling Thrombopoiesis in Zebrafish." Thesis, University of North Texas, 2015. https://digital.library.unt.edu/ark:/67531/metadc822768/.

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Thrombocytes are functional equivalents of mammalian platelets and also possess megakaryocyte features. It has been shown earlier that hox genes play a role in megakaryocyte development. Our earlier microarray analysis showed five hox genes, hoxa10b, hoxb2a, hoxc5a, hoxc11b and hoxd3a, were upregulated in zebrafish thrombocytes. However, there is no comprehensive study of genome wide scan of all the hox genes playing a role in megakaryopoiesis. I first measured the expression levels of each of these hox genes in young and mature thrombocytes and observed that all the above hox genes except hoxc11b were expressed equally in both populations of thrombocytes. hoxc11b was expressed only in young thrombocytes and not in mature thrombocytes. The goals of my study were to comprehensively knockdown hox genes and identify the specific hox genes involved in the development of thrombocytes in zebrafish. However, the existing vivo-morpholino knockdown technology was not capable of performing such genome-wide knockdowns. Therefore, I developed a novel cost- effective knockdown method by designing an antisense oligonucleotides against the target mRNA and piggybacking with standard control morpholino to silence the gene of interest. Also, to perform knockdowns of the hox genes and test for the number of thrombocytes, the available techniques were both cumbersome or required breeding and production of fish where thrombocytes are GFP labeled. Therefore, I established a flow cytometry based method of counting the number of thrombocytes. I used mepacrine to fluorescently label the blood cells and used the white cell fraction. Standard antisense oligonucleotide designed to the central portion of each of the target hox mRNAs, was piggybacked by a control morpholino and intravenously injected into the adult zebrafish. The thrombocyte count was measured 48 hours post injection. In this study, I found that the knockdown of hoxc11b resulted in increased number of thrombocytes and knockdown of hoxa10b, hoxb2a, hoxc5a, and hoxd3a showed reduction in the thrombocyte counts. I then screened the other 47 hox genes in the zebrafish genome using flow sorting method and found that knockdown of hoxa9a and hoxb1a also resulted in decreased thrombocyte number. Further, I used the dye DiI, which labels only young thrombocytes at specific concentrations and observed that the knockdown of hoxa10b, hoxb2a, hoxc5a, hoxd3a, hoxa9a and hoxb1a, lead to a decrease in young thrombocytes; whereas hoxc11b knockdown lead to increase in number of young thrombocytes. Using bromodeoxyuridine, I also showed that there is increase in release of young thrombocytes into peripheral circulation in hoxc11b knockdown fish which suggests that hoxc11b significantly promotes cell proliferation rather effecting apoptosis. In conclusion, I found six hox genes that are positive regulators and one hox gene is a negative regulator for thrombocyte development.
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Williams, Christopher M. "Protein kinase Ca in bone eevelopment, thrombopoiesis and thrombosis." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526061.

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Hall, Mark Andrew. "Characterisation of the interleukin 11 receptor complex." Thesis, University of Birmingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396241.

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Fock, Ee-Ling Clinical School St George Hospital Faculty of Medicine UNSW. "Molecular regulation and enhancement of megakaryopoiesis and thrombopoiesis by the p45 subunit of NF-E2." Publisher:University of New South Wales. Clinical School - St George Hospital, 2008. http://handle.unsw.edu.au/1959.4/42885.

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Megakaryocytes (MKs) are a rare population of haematopoietic cells, which produce platelets. Platelet production is a complex process that is tightly regulated at the transcriptional level by lineage specific transcription factors such as p45 NF-E2. Understanding how transcriptional regulators operate is imperative to advance our knowledge of disease pathophysiology and to propose novel treatment options. Therefore, the aims of this study were to: i) study the effects of p45 NF-E2 overexpression on various stages of megakaryopoiesis; (ii) elucidate the nuclear transport mechanisms of p45 NF-E2; and iii) determine the impact of a p45 NF-E2 modification called SUMOylation on thrombopoiesis. Exogenous p45 NF-E2 was overexpressed in haematopoietic cells in culture and various aspects of megakaryopoiesis were examined. Overexpression of p45 NF-E2 enhanced multiple stages of MK differentiation such as colony forming unit (CFU)-MK formation and terminal MK maturation. Most importantly, p45 NF-E2 overexpression resulted in significant increases in proplatelet and functional platelet production in vitro. This latter result was confirmed in vivo using lethally irradiated mice transplanted with cells that overexpressed p45 NF-E2. Unexpectedly, the enhancement of MK differentiation was at the expense of myeloid development and, for the first time, identified p45 NF-E2 as a negative regulator of myeloid differentiation. Secondly, we determined the nuclear localisation signal of p45-NF-E2 and the pathway responsible for nuclear import. We also investigated the importance of p45 NF-E2 nuclear import in thrombopoiesis. Finally, we showed that p45 NF-E2 is modified mainly by SUMO-2/3 in bone marrow cells and this process is involved in the transcriptional activation of MK-specific genes and platelet release. Taken together, these results suggest that enforced expression of p45 NF-E2 selectively enhances many aspects of MK differentiation including early and terminal MK maturation, proplatelet formation and platelet release. Equally important, this thesis also indicates that white blood cell differentiation may be inhibited by p45 overexpression, while molecular processes such as the nuclear import and SUMOylation of p45 NF-E2 are vital for thrombopoiesis. These observations will facilitate subsequent studies into the feasibility of manipulating p45 NF-E2 protein levels for the treatment of conditions such as thrombocytopaenia and other platelet disorders.
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Zhang, Zhe [Verfasser], and Steffen [Akademischer Betreuer] Massberg. "The role of leukocyte-megakaryocyte interactions during the thrombopoiesis / Zhe Zhang ; Betreuer: Steffen Massberg." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/1238016936/34.

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Zhang, Lin [Verfasser], Steffen [Akademischer Betreuer] Massberg, Stefan [Akademischer Betreuer] Engelhardt, and Dirk [Akademischer Betreuer] Busch. "The effect of Sphingosine 1-phosphate (S1P) on thrombopoiesis / Lin Zhang. Gutachter: Stefan Engelhardt ; Dirk Busch. Betreuer: Steffen Massberg." München : Universitätsbibliothek der TU München, 2012. http://d-nb.info/1020915080/34.

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Eeuwijk, Judith Martina Maria van [Verfasser], and Bernhard [Gutachter] Nieswandt. "Studies on thrombopoiesis and spleen tyrosine kinase-mediated signaling in platelets / Judith Martina Maria van Eeuwijk ; Gutachter: Bernhard Nieswandt." Würzburg : Universität Würzburg, 2018. http://d-nb.info/1151128600/34.

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Choudry, Fizzah Aziz. "Novel insights into megakaryopoiesis, thrombopoiesis and acute coronary thrombosis : transcriptome profiling of the haematopoietic stem cell, megakaryocyte and platelet." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/283252.

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The aim of this project was to investigate the transcriptome of human haematopoietic stem cells (HSCs), megakaryocytes and platelets to gain insights into steady state and accelerated thrombopoiesis that occurs in states of haemostatic demand and in thrombosis by applying these findings to the pathological setting of acute coronary thrombosis. To investigate transcriptional heterogeneity within the human HSC population, single cell RNA sequencing was performed in human bone marrow HSCs. Transcriptionally distinct subpopulations were identified including two megakaryocyte biased subsets with potentially differing functional relevance. Both populations expressed megakaryocyte specific transcripts, one of which also co-expressed common myeloid and megakaryocyte-erythroid progenitor transcripts while the other did not. This study represents the first interrogation of the human bone marrow megakaryocyte transcriptome. Cells were collected from healthy human bone marrow and analysed by low input and single cell RNA sequencing. To identify novel drivers of megakaryocyte maturation, the human bone marrow megakaryocyte transcriptome was compared to that of megakaryocytes cultured from human CD34+ cells, a process known to generate immature megakaryocytes. Transcriptional signatures associated with increasing megakaryocyte ploidy were then investigated. Increasing megakaryocyte ploidy level was found to be associated with an upregulation of transcripts involved in translation and protein processing as well as expression of a number of transmembrane receptors which might have functional relevance. Finally, the pathological setting of acute coronary thrombosis was used as a model for accelerated thrombopoiesis. Megakaryocyte and platelet transcriptomes were compared between patients with acute myocardial infarction (AMI) as well as severe coronary disease and a control group. The transcriptional signature relating to disease compared to control in megakaryocytes included upregulation of platelet activation related transcripts in megakaryocytes isolated from patients with AMI and severe coronary artery disease.
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Meyer, Imke [Verfasser]. "The functional blood platelet and its biogenesis : Biochemical and cell biological analysis of thrombopoiesis in vitro, in situ and in vivo / Imke Meyer." Berlin : Freie Universität Berlin, 2013. http://d-nb.info/1031666958/34.

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McIntosh, Bryan James. "Regulation of thrombopoietin in bone marrow." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3284334.

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Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed January 9, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 50-58).
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Books on the topic "Thrombopoiesis"

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Kuter, David J., Pamela Hunt, William Sheridan, and Dorothea Zucker-Franklin, eds. Thrombopoiesis and Thrombopoietins. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1.

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Thrombopoiesis and Thrombopoietins. Springer My Copy UK, 1996.

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J, Kuter David, ed. Thrombopoiesis and thrombopoietins: Molecular, cellular, preclinical, and clincial biology. Totowa, N.J: Humana Press, 1997.

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(Editor), David Kuter, Pamela Hunt (Editor), William P. Sheridan (Editor), and Dorothea Zucker-Franklin (Editor), eds. Thrombopoiesis and Thrombopoietins: Molecular, Cellular, Preclinical, and Clinical Biology. Humana Press, 1996.

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David J. Kuter Pamela Hunt. Thrombopoiesis and Thrombopoietins: Molecular, Cellular, Preclinical, and Clinical Biology. Humana Press, 2011.

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Thrombopoietin: From Molecule to Medicine. AlphaMED Press, 1998.

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Thrombopoietin: From Molecule to Medicine. AlphaMED Press, 1998.

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J, Murphy Martin, and Kuter David J, eds. Thrombopoietin: From molecule to medicine. Miamisburg, Ohio: AlphaMed Press, 1998.

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Curry, Nicola, and Raza Alikhan. Normal platelet function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0281.

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The platelet is a small (2–4 µm in diameter), discoid, anucleate cell that circulates in the blood. In health, it plays a vital role in haemostasis, and in disease it contributes to disorders of bleeding and thrombosis. Platelets are produced from the surface of megakaryocytes in the bone marrow, under tight homeostatic control regulated by the cytokine thrombopoietin. Platelets have a lifespan of approximately 7–10 days, and usually circulate in the blood stream in a quiescent state. Intact, undamaged vessel walls help to maintain platelets in this inactive state by releasing nitric oxide, which acts both to dilate the vessel wall and to inhibit platelet adhesion, activation, and aggregation. After trauma to the blood vessel wall, platelets are activated and, acting in concert with the endothelium and coagulation factors, form a stable clot. This chapter addresses platelet structure and function, and the response of platelets to vessel injury.
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Book chapters on the topic "Thrombopoiesis"

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Jackson, Carl W., Julie T. Arnold, Tamara I. Pestina, and Paula E. Stenberg. "Megakaryocyte Biology." In Thrombopoiesis and Thrombopoietins, 3–39. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_1.

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Hoffman, Ronald. "The Role of Other Hemopoietic Growth Factors and the Marrow Microenvironment in Megakaryocytopoiesis." In Thrombopoiesis and Thrombopoietins, 165–78. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_10.

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Gurney, Austin L., and Frederic J. de Sauvage. "Structure of Thrombopoietin and the Thrombopoietin Gene." In Thrombopoiesis and Thrombopoietins, 181–88. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_11.

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Shivdasani, Ramesh A. "Transcription Factors in Megakaryocyte Differentiation and Gene Expression." In Thrombopoiesis and Thrombopoietins, 189–202. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_12.

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Foster, Donald, and Pamela Hunt. "The Biological Significance of Truncated and Full-Length Forms of Mpl Ligand." In Thrombopoiesis and Thrombopoietins, 203–14. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_13.

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Debili, Najet, Elisabeth Cramer, Françoise Wendling, and William Vainchenker. "In Vitro Effects of Mpl Ligand on Human Hemopoietit Progenitor Cells." In Thrombopoiesis and Thrombopoietins, 217–35. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_14.

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Zucker-Franklin, Dorothea. "Effect of Cytokines on the Development of Megakaryocytes and Platelets." In Thrombopoiesis and Thrombopoietins, 237–55. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_15.

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Kaushansky, Kenneth, Virginia C. Broudy, and Jonathan G. Drachman. "The Thrombopoietin Receptor, Mpl, and Signal Transduction." In Thrombopoiesis and Thrombopoietins, 257–70. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_16.

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Choi, Esther. "Regulation of Proplatelet and Platelet Formation In Vitro." In Thrombopoiesis and Thrombopoietins, 271–84. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_17.

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Harker, Laurence A., Ulla M. Marzec, and Christopher F. Toombs. "In Vitro Effects of Mpl Ligands on Platelet Function." In Thrombopoiesis and Thrombopoietins, 285–97. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_18.

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Conference papers on the topic "Thrombopoiesis"

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Marini, Irene, Jan Zlamal, Christoph Faul, Ursula Holzer, Stefanie Hammer, Lisann Pelzl, Wolfgang Bethge, Karina Althaus, and Tamam Bakchoul. "Autoantibody-Mediated Desialylation Impairs Human Thrombopoiesis and Platelet Life Span." In Hamburger Hämophilie Symposion Hamburg, Germany. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1721592.

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Gugliotta, L., S. Macchi, L. Catani, M. Mattioli Belmonte, L. Gaggioli, and S. Tura. "EVALUATION OF THROMBOPOIESIS IN ESSENTIAL THROMBOCYTHAEMIA BEFORE AND AFTER α-INTERFERON TREATMENT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644579.

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The α-interferon (α-IFN) has been shown efficacious in controlling thrombocytosis in chronic myeloproliferative disorders. In order to better understand the mechanisms by which this effect is produced, the main parameters of thrombopoiesis have been evaluated in 8 patients with Essential Thrombocythaemia (ET)just before and at the end of induction therapy with α-IFN. The patients, 2 males and 6 females, 17-54 years old, at diagnosis or at least 3 months off cytotoxic drugs, received α-IFN (Roferon A-Roche) s.c. at a daily dose of 3 × 106 IU for 6-13 weeks. The baseline platelet count of 993±266×109/1 fell, after treatment, to a value of 377±96×109 /1. The histological analysis of the bone marrow showed that the number of megakaryocytes (MK), initially 5-15 times the normal value (N), decreased to a value of 3-6 × N, while the MK volume resulted always high. The "in vitro" study of megakaryocytopoiesis, by the plasma-clot culture technique, documented a significant decrease of the number of MK colonies (from 73±18 to 29±15; p <0.0001). The half life-span of autologous platelets labelled withulIn-oxine remained unchanged (97±22 and 101±25 hours before and after therapy, respectively), while the platelet function abnormalities (hypo-aggregation, storage pool deficiency, etc) appeared less severe after treatment.It is concluded that in ET the α-IFN therapy is able to normalize the platelet count mainly or exclusively by a decrease of platelet production.The work was supported in part by grant of National Research Council (CNR), special Project Oncology No 85.02200.44.
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Heynen, M. J., R. L. Verwilghen, and J. Vermylen. "DOES THE MEGAKARYOCYTE CYTOSKELETON REGULATE IRROMBOPOIESIS?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643544.

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A widely held view of thrombopoiesis is that platelets arise from fragmentation of the periphery of mature megakaryocytes (MK’s). Evidence against this concept was provided by Zucker-Franklin, who showed that platelet plasma membrane is different from that of the MK (freeze-fracture, membrane antigens). Several authors have described contractile processes in MK’sWe have performed detailed electronmicroscopic studies of the numerous small MK's of a subject with congenital macrothrombocytopenia. In the young granular MK’s a central zone with organelles and a thick peripheral zone without organelles can be observed. The absence of elements of the demarcation system in the peripheral zone argues against derivation of the demarcation system from the megakaryocyte plasma membrane. In the mature granular MK’s the heart of the central zone is not occupied by the nucleus, but by an area, free of organelles and membranes, containing fibrillar structures and the centrioles. Elements of the demarcation system, delineating platelet territories, radiate from this fibril-rich area, but do not extend into the very thin peripheral zone. In the platelet producing MK’s the peripheral zone is thicker and the central fibril-rich area is surrounded by separated platelet territories. The peripheral zone shows several openings. In the old MK’s the nucleus is only surrounded by a markedly thickened peripheral zone, which seems to result from contraction of the more extended peripheral zone of the platelet producing MK's.From these observations we conclude that, at least in this patient, platelets are formed inside the MK and are extruded through openings of the peripheral zone. Further studies with cytoskeleton markers are required to confirm that (!) the fibril-rich heart governs the organisation of platelet territories and (2) that platelet extrusion results from contraction of the peripheral zone, the latter however not giving rise to platelets.
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Rambhia, S. H., C. Ji, L. Scudder, J. Wainer, M. Monaghan, A. Dhundale, D. V. Gnatenko, and W. F. Bahou. "Dissection of the thrombopoietic transcriptome using a platelet specific microarray." In 2007 IEEE 33rd Annual Northeast Bioengineering Conference. IEEE, 2007. http://dx.doi.org/10.1109/nebc.2007.4413346.

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Margraf, A., C. Liu, and A. Zarbock. "Thrombopoietin levels in sepsis and septic shock - a meta-analysis." In 65th Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1728178.

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Jackson, Walter, Andrea M. Mastro, and Donna M. Sosnoski. "Abstract 3265: Thrombopoietin and megakaryocytes in breast cancer metastasis to bone." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3265.

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Korde, A., F. Ahangari, M. Haslip, G. L. Chupp, J. Pober, A. Gonzalez, J. L. Gomez, and S. Takyar. "Endothelial Thrombopoietin Receptor Regulates the Severity of Type 2 Inflammation by Controlling Platelet-Eosinophil Engagement." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7635.

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Jeong, Jee-Yeong, and K. Gary Vanasse. "Abstract 4267: Eltrombopag, a non-peptide thrombopoietin receptor agonist, enhances theex vivoexpansion of human hematopoietic stem cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4267.

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Tanaka, Hiroki, Kie Horioka, Masahiro Yamamoto, Katsuhiro Okuda, Masaru Asari, Katsuhiro Okuda, Seiji Ohtani, Kosuke Yamazaki, Keiko Shimizu, and Katsuhiro Ogawa. "Abstract 4803: Over-production of thrombopoietin in the liver of transgenic mice with liver-specific human BrafV600E expression." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4803.

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