Relevant bibliographies by topics / Thrombopoietin

Academic literature on the topic 'Thrombopoietin'

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Published: 4 June 2021
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Journal articles on the topic "Thrombopoietin"

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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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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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Andemariam, Biree, Bethan Psaila, and James B. Bussel. "Novel Thrombopoietic Agents." Hematology 2007, no. 1 (January 1, 2007): 106–13. http://dx.doi.org/10.1182/asheducation-2007.1.106.

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AbstractThrombocytopenia is a primary manifestation of immune thrombocytopenic purpura (ITP) and may occur as a result of hepatitis C, malignancy, and treatment with chemotherapy. There is a need for additional means to treat thrombocytopenia in these settings. Recombinant thrombopoietin-like agents became available after the cloning of thrombopoietin in 1994. In clinical trials, these agents showed some efficacy in chemotherapy-induced thrombocytopenia, but their use was ultimately discontinued due to the development of neutralizing antibodies that cross-reacted with endogenous thrombopoietin and caused thrombocytopenia in healthy blood donors and other recipients. Subsequently, “second-generation” thrombopoietic agents without homology to thrombopoietin were developed. In the past 5 years, these second-generation thrombopoeitic growth factors have undergone substantial clinical development and have demonstrated safety, tolerability and efficacy in subjects with ITP and hepatitis C–related thrombocytopenia. These completed studies, many of which are available only in abstract form, and other ongoing studies suggest that thrombopoietic agents will enhance the hematologist’s ability to manage these and other causes of thrombocytopenia.
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Oda, A., Y. Miyakawa, BJ Druker, K. Ozaki, K. Yabusaki, Y. Shirasawa, M. Handa, et al. "Thrombopoietin primes human platelet aggregation induced by shear stress and by multiple agonists." Blood 87, no. 11 (June 1, 1996): 4664–70. http://dx.doi.org/10.1182/blood.v87.11.4664.bloodjournal87114664.

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Recombinant thrombopoietin has been reported to stimulate megakaryocytopoiesis and thrombopoiesis and it may be quite useful to treat patients with low platelet counts after chemotherapy. As little is known regarding the possible activation of platelets by thrombopoietin, we examined the effects of thrombopoietin on platelet aggregation induced by shear stress and various agonists in native plasma. Using hirudin as an anticoagulant, thrombopoietin (1 to 100 ng/mL) enhanced platelet aggregation induced by 2 micromol/L adenosine- diphosphate (ADP) in a dose dependent fashion. The enhancement was not affected by treatment of platelets with 1 mmol/L aspirin plus SQ-29548 (a thromboxane antagonist, 1 micromol/L) but was inhibited by a soluble form of the thrombopoietin receptor, suggesting that the enhancement was mediated by the specific receptors and does not require thromboxane production. Epinephrine (1 micromol/L), which does not induce platelet aggregation in hirudin platelet rich plasma (PRP), did so in the presence of thrombopoietin (10 ng/mL). Thrombopoietin (10 ng/mL) also enhanced or primed platelet aggregation induced by collagen (0.5 micron.mL),. thrombin, serotonin, and vasopressin. Thrombopoietin does not induce any rise in cytosolic ionized calcium concentration nor activation of protein kinase C, as estimated by phosphorylation of preckstrin, indicating that the priming effects of thrombopoietin does not require those processes. The ADP- or thrombin-induced rise in cytosolic ionized calcium concentration was not enhanced by thrombopoietin (100 ng/mL). Further, shear (ca. 90 dyn/cm2)-induced platelet aggregation was also potentiated by thrombopoietin. The priming effect on epinephrine-induced platelet aggregation in hirudin PRP was unique to thrombopoietin, with no effects seen using interleukin-6 (IL-6), IL-11, IL-3, erythropoietin, granulocyte-colony stimulating factor, granulocyte macrophage-colony stimulating factor, or c-kit ligand. These data indicate that monitoring of platelet functions may be necessary in the clinical trials of thrombopoietin.
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Miyakawa, Yoshitaka, Brian Druker, Katsutoshi Ozaki, Hideya Ohashi, Takashi Kato, Hiroshi Miyazaki, Makoto Handa, Kenji Ikebuchi, Yasuo Ikeda, and Atsushi Oda. "Thrombopoietin-Induced Signal Transduction and Potentiation of Platelet Activation." Thrombosis and Haemostasis 82, no. 08 (1999): 377–84. http://dx.doi.org/10.1055/s-0037-1615856.

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IntroductionThe presence of thrombopoietin, a humoral regulator of megakaryopoiesis and thrombopoiesis, had been suggested for years,1 however, some investigators were skeptical about the existence of such a factor. Modern studies of thrombopoietin begin with the cloning of c-mpl (the cellular counterpart of the v-mpl oncogene) and its cognate ligand genes. Following the cloning of the c-mpl proto-oncogene,2 Methia et al3 found that, in the presence of oligonucleotides antisense to the gene, CD34+ cells developed into megakaryocytic precursors less efficiently. As the development into other lineage was nearly intact, it was reasonably argued that the c-mpl protein may be the receptor for a thrombopoietin-like factor.3 This study inspired numerous investigations, which culminated in the cloning of the thrombopoietin gene in 1994.1, 4-8
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Miyakawa, Y., A. Oda, BJ Druker, T. Kato, H. Miyazaki, M. Handa, and Y. Ikeda. "Recombinant thrombopoietin induces rapid protein tyrosine phosphorylation of Janus kinase 2 and Shc in human blood platelets." Blood 86, no. 1 (July 1, 1995): 23–27. http://dx.doi.org/10.1182/blood.v86.1.23.bloodjournal86123.

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A cDNA for the thrombopoietin has been cloned by several groups. The recombinant thrombopoietin has been reported to stimulate the megakaryocytopoiesis and thrombopoiesis. Little is known regarding the molecular basis of its effects. To elucidate the molecular mechanism involved in signal transduction, we have investigated the effects of thrombopoietin on platelet tyrosine phosphorylation. We report here that thrombopoietin induced time- and dose-dependent tyrosine phosphorylation of several proteins including Janus kinase 2 (Jak2) and a 52-kD protein, Shc, in human blood platelets. Both Jak2 and Shc were tyrosine phosphorylated within 15 seconds after stimulation. The tyrosine phosphorylation of Jak2 was accompanied by increased kinase activity, whereas Shc tyrosine phosphorylation induced its association with a 25-kD protein, Grb2. Thus, our data suggest that Jak2, Shc, and Grb2 may be involved in signal transduction after ligand binding to c- mpl in human platelets.
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Underhill, Craig R., and Russell L. Basser. "Thrombopoietin." BioDrugs 11, no. 4 (1999): 261–76. http://dx.doi.org/10.2165/00063030-199911040-00005.

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Kaushansky, Kenneth. "Thrombopoietin." Trends in Endocrinology & Metabolism 8, no. 2 (March 1997): 45–50. http://dx.doi.org/10.1016/s1043-2760(96)00269-x.

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Kaushansky, Kenneth. "Thrombopoietin." New England Journal of Medicine 339, no. 11 (September 10, 1998): 746–54. http://dx.doi.org/10.1056/nejm199809103391107.

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Thompson, Clare. "Thrombopoietin." Lancet 343, no. 8913 (June 1994): 1630. http://dx.doi.org/10.1016/s0140-6736(94)93079-1.

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Dissertations / Theses on the topic "Thrombopoietin"

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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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Sangkhae, Veena. "The role of thrombopoietin signalling in JAK2V617F-positive myeloproliferative neoplasms." Thesis, University of York, 2015. http://etheses.whiterose.ac.uk/9669/.

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Thrombopoietin (TPO) is the primary regulator of megakaryocyte development, regulating proliferation and differentiation in addition to the number of circulating platelets through binding to and stimulation of the cell surface receptor MPL. Activating mutations in MPL constitutively stimulate downstream signalling pathways, leading to aberrant haematopoiesis and contribute to development of myeloproliferative neoplasms (MPNs). Several studies have mapped the tyrosine residues within the cytoplasmic domain of MPL that mediate these cellular signals; however, secondary signalling pathways are incompletely understood. Additionally, the identification of the JAK2V617F mutation has profoundly increased our understanding of MPNs and although a role has been implicated in vitro, the in vivo role of MPL in JAK2V617F-positive MPNs has yet to be determined. In this thesis, a novel signalling pathway for the negative regulation of TPO signalling was identified whereby MPLY591 is phosphorylated resulting in association of SYK which negatively regulates TPO-mediated ERK1/2 signalling. Additionally, genetic manipulation of an in vivo JAK2V617F-positive MPN mouse model led to the identification of MPL as an essential molecular component for development of JAK2V617F-postive MPNs. In the absence or reduction of MPL, the disease fails to develop. However, removal of the cytokine, TPO, was unable to prevent the disease from developing. These findings provide novel insights not only into regulation of TPO-signalling but also the role of TPO and MPL in JAK2V617F-positive MPN disease pathogenesis. Identification of the role of MPL in MPN pathogenesis, as well as insights into additional regulatory pathways, contributes to our understanding of normal and pathological TPO signalling. These new insights also provide a basis for development of novel therapeutics for the treatment of MPNs and other diseases resulting from aberrant of TPO signalling.
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Schulze, Harald. "Biochemische Untersuchungen zur Signaltransduktion des Thrombopoietin-Rezeptors c-Mpl in Thrombozyten." [S.l.] : [s.n.], 1999. http://deposit.ddb.de/cgi-bin/dokserv?idn=957851413.

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Fleschutz, Frederik. "Bestimmung der Serumspiegel von Thrombopoietin und Erythropoietin bei Erst-, Vollblut- und Thrombozytapharesespendern /." Düsseldorf, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253967.

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Barbieri, Daniela. "Role of thrombopoietin in DNA repair an genomic integrity in hematopoietic stem cells." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB002.

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Le maintien de l'intégrité génomique est crucial pour la préservation du potentiel des cellules souches hématopoïétiques (CSH). Les lésions de l'ADN dans les CSH sont associées à une capacité réduite à reconstituer l'hématopoïèse, à altérer le potentiel de différentiation et à accroître le risque de développer des tumeurs myéloïdes. Les éléments rétrotransposables (ER), se propageant dans le génome à travers un ARN intermédiaire, ont été associés à la perte d'auto-renouvellement, au vieillissement et aux dommages à l'ADN. Cependant, leur rôle dans les CSH n'avait pas été abordé. Dans cette étude, nous avons constaté que les CSH expriment des niveaux élevés d'ARNm de plusieurs ER comprenant des rétrovirus endogènes (ERV) et des L1 (LINE-1: Long Interspersed Nuclear Elements 1). Leur expression augmente avec l'irradiation. En utilisant des souris transgéniques L1-EGFP, on a montré que la rétrotransposition de L1 se produit dans les CSH in vivo. En outre, les inhibiteurs de la transcriptase inverse Efavirenz et ddC sauve à la fois les CSH des dommages persistants à l'ADN induit par l’irradiation et de la perte de prolifération in vitro. Ceci démontre que la rétrotransposition endogène joue un rôle important dans l'instabilité génomique de CSH induite par l’irradiation et dans leur perte de fonction. Nous avons précédemment montré que la thrombopoïétine (TPO), un facteur d'auto-renouvellement critique pour le CSH, limite les lésions de l'ADN induites par l’irradiation en améliorant la réparation de l'ADN. Nous avons découvert que le traitement par TPO empêche également l'expression et la mobilisation d’ER induite par l’irradiation. Nous avons aussi constaté que l’expression et la retrotransposition de L1 augmente dans les CSH provenant de souirs Mpl-/- et L1-EGFPxMpl-/-. Cela montre que la signalisation TPO in vivo est nécessaire pour restreindre l’expression et la retrotransposition d’ER dans les CSH au niveau basal et dans des conditions de stress. L'analyse transcriptomique a révélé que la TPO induit une réponse d'expression génique antivirale d'interféron (IFN) de type I dans les CSH. En utilisant des souris déficientes en STAT1/STAT2, nous démontrons que cette réponse est dépendante à la fois de STAT1 et de STAT2 et est requise pour l'inhibition de l'expression d’ER. En conclusion, cette étude montre que les ER représentent une importante source d’instabilité génomique dans les CSH. Les CSH sont capables de monter une réponse antivirale en réponse à la TPO comme un nouveau mécanisme pour limiter les dommages à l'ADN. Bien que la sécrétion constitutive d'IFN-I se produise chez des souris saines, les IFN sont produits abondamment principalement pendant les infections. Ainsi, la réponse d'expression de gène d'IFN induite par la TPO peut représenter un signal constitutif important et CSH-dédié; permettant à ces cellules de résister aux lésions de l'ADN induites par ER, tout en préservant leur capacité d'auto-renouvellement
Maintenance of genomic integrity is crucial for the preservation of hematopoietic stem cell (HSC) potential. DNA damage in HSCs is associated with reduced ability to reconstitute hematopoiesis, altered lineage potential and accrued risk of developing myeloid malignancies. Retrotransposable elements (RE), spreading in the genome through an RNA intermediate, have been associated with loss of self-renewal, aging and DNA damage. However, their role in HSCs has not been addressed. In this study, we found that HSCs express high mRNA levels of several REs, including evolutionary recent long interspersed element-1 (L1) and endogenous retroviruses (ERV). Their expression further increases upon total body irradiation (TBI). Using L1EGFP transgenic reporter mice, we show that productive L1 retransposition occurs in HSCs in vivo. Furthermore, the reverse transcriptase inhibitors Efavirenz and ddC rescue TBI-induced both persistent DNA damage and HSC loss of proliferation in vitro. This demonstrates that endogenous retrotransposition plays an important role in TBI-induced HSC genomic instability and their loss of function. We have previously shown that thrombopoietin (TPO), a critical HSC self-renewal factor limits TBI-induced HSC DNA damage by improving DNA repair. We found that TPO treatment also prevents TBI-induced RE expression and mobilization. In addition, L1 expression and retrotransposition are increased in Mpl-/- and L1-EGFPxMpl-/- HSCs, showing that TPO signaling in vivo is required to restrain RE in HSCs, under both steady state and stress conditions. Transcriptomic analysis revealed that TPO induces an anti-viral, interferon (IFN) type-I like, gene expression response in HSCs. Using STAT1/STAT2-deficient mice, we demonstrate that this response is dependent on both STAT1 and STAT2 and is required for TPO-mediated RE expression inhibition in HSCs. Overall, this study shows that REs represent an important HSC intrinsic source of genomic instability and uncovers the ability of HSCs to mount an anti-viral innate immune state in response to TPO as a novel mechanism to minimize DNA damage. Although constitutive IFN-I secretion occurs in healthy mice, IFNs are produced abundantly mainly during infections. Thus, TPO-induced IFN gene expression response may represent an important constitutive, and HSC-dedicated, signal allowing HSCs to resist RE-induced DNA damage while preserving their self-renewal ability
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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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Cheung, Manyee. "Investigation of megakaryocytes from normal and myeloproliferative bone marrow biopsies." Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343012.

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Bulla, Camilo [UNESP]. "Seqüenciamento e expressão da trombopoietina canina." Universidade Estadual Paulista (UNESP), 2005. http://hdl.handle.net/11449/103774.

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Kafka, Isabell Katharina Anna. "Bestimmung der Serumkonzentration von Thrombopoietin bei Patienten mit Chemotherapie-, perioperativ- und ideopathisch-bedingter Thrombozytopenie sowie In-vitro-Untersuchungen der Thrombopoietin-Clearance von Thrombozyten und MEG-01-Zellen zur Optimierung der Behandlung thrombozytopenischer Patienten /." Düsseldorf, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000254041.

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Barnes, Calvin Langston Toure. "C-mpl Expression in Osteoclast Progenitors: A Novel Role for Thrombopoietin in Regulating Osteoclast Development." Yale University, 2006. http://ymtdl.med.yale.edu/theses/available/etd-06262006-123750/.

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A new paradigm has evolved in which multiple regulatory interactions between the skeletal and hematopoietic systems have been identified. Previous studies have demonstrated that megakaryocytes (MK) play a dual role in skeletal homeostasis by stimulating osteoblast proliferation and simultaneously inhibiting osteoclast (OC) development. Here we identify a novel regulatory pathway in which the main MK growth factor, thrombopoietin (TPO), directly regulates osteoclastogenesis. To study the role of TPO in OC development, spleen or bone marrow (BM) cells (2x10[exponent]6 cells/ml) or BM macrophages (BMM, 1x10[exponent]5 cells/ml) from C57BL/6 mice , as a source of OC precursors, were cultured with M-CSF (30 ng/ml) and RANKL (50 ng/ml) to induce OC formation. TPO (0.1-1000 ng/ml) and/or primary MK (0-0.5%), derived from C57BL/6 fetal livers, were titrated into these cultures and OC were identified as tartrate resistant acid phosphatase positive (TRAP+) giant cells with >3 nuclei. There was a significant, up to 15-fold reduction in OC formed when MK were added to all OC generating cultures, p < 0.001. Moreover, if OC generating cultures did not contain MK or MK progenitors, TPO treatment significantly enhanced OC formation up to six-fold, p < 0.01. This data demonstrates that MK are responsible for the inhibition of OC formation and that in cultures containing MK or MK progenitors such as BM or spleen cells, that TPO acts indirectly to inhibit OC formation by stimulating megakaryopoiesis, whereas in the absence of MK or MK progenitors TPO directly enhances OC formation. This conclusion is further supported by Real-Time PCR data which demonstrates that OC progenitors express c-mpl, the TPO receptor, albeit at low levels when compared to expression of c-mpl on MK. Finally, we have begun to dissect the c-mpl signaling pathway in OC progenitors. We have found that TPO induces tyrosine phosphorylation of several specific cellular proteins in the JAK/STAT pathway. Thus, TPO acts in a somewhat paradoxical manner by inhibiting OC formation through the stimulation of MK, while simultaneously playing a direct role in enhancing osteoclastogenesis.
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Books on the topic "Thrombopoietin"

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

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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 "Thrombopoietin"

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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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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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Eaton, Dan. "The Purification and Cloning of Human Thrombopoietin." In Thrombopoiesis and Thrombopoietins, 135–41. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_8.

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Kuter, David J., Hiroshi Miyazaki, and Takashi Kato. "The Purification of Thrombopoietin from Thrombocytopenic Plasma." In Thrombopoiesis and Thrombopoietins, 143–64. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_9.

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Nichol, Janet Lee. "Serum Levels of Thrombopoietin in Health and Disease." In Thrombopoiesis and Thrombopoietins, 359–75. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_22.

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de Sauvage, Frederic J., and Mark W. Moore. "Genetic Manipulation of Mpl Ligand and Thrombopoietin In Vivo." In Thrombopoiesis and Thrombopoietins, 349–56. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_21.

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Kaushansky, Kenneth, Nancy Lin, Angelika Grossmann, Katherine Sprugel, Ewa Sitnicka, and Virginia Broudy. "Thrombopoietin." In Molecular Biology of Hematopoiesis 5, 477–83. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0391-6_58.

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Wei, Ping. "Thrombopoietin Factors." In Hematopoietic Growth Factors in Oncology, 75–93. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7073-2_5.

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Kuter, David J. "Thrombopoietin Factors." In Hematopoietic Growth Factors in Oncology, 125–51. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-747-5_7.

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Tomiyama, Yoshiaki. "Thrombopoietin Receptor Agonists." In Autoimmune Thrombocytopenia, 171–81. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4142-6_17.

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Conference papers on the topic "Thrombopoietin"

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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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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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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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