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Leng, Henry Martin John. "The biogenesis of erythropoietin during inflammation". Doctoral thesis, University of Cape Town, 1995. http://hdl.handle.net/11427/27051.
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Anaemia frequently accompanies chronic inflammatory diseases like rheumatoid arthritis and cancer. It is postulated to result primarily from the suppression of erythropoiesis by inflammatory cytokines. A contributing factor could be the inhibition of erythropoietin synthesis which may also be mediated by cytokines. Erythropoietin is the hormone which regulates erythropoiesis. The aims of this project were to investigate whether cytokines can indeed suppress erythropoietin production, and to determine whether the erythropoietin response in experimental models of acute and chronic inflammation was appropriate for the associated anaemia. Macrophage-conditioned medium, interleukin-1β, interleukin-6, tumour necrosis factor-α, and neopterin were assayed for inhibition of erythropoietin synthesis by HepG2 cells in culture. All, except neopterin, effected dose-dependent reductions in the secretion of the hormone. Interleukin-1β and tumour necrosis factor-α down-regulated erythropoietin gene transcription, whereas interleukin-6 inhibited a post-transcriptional process. Rats with acute inflammation developed a mild anaemia which evoked an increase in their serum levels of erythropoietin. The serum erythropoietin levels were optimal, since rats with acute inflammation and severe phenylhydrazine-induced anaemia did not have lower levels of the hormone than controls with a similar degree of anaemia, but without acute inflammation. Erythropoietin is, therefore, not an acute phase reactant. Mice with cancer developed a progressive anaemia which was not due to bone marrow invasion by tumour cells. During the first fourteen days after inoculating them with cancer cells, the mice responded by increasing their serum levels of erythropoietin as the anaemia worsened. The erythropoietin response was appropriate when compared to mice with the same degree of phenylhydrazine-induced anaemia. Erythropoietin levels measured in mice with tumours older than fourteen days were significantly lower than those of control mice with the same degree of experimental anaemia. These animals were very cachectic, suggesting that a blunted erythropoietin response may depend on disease activity.
2
Afrasiabi, Morteza. "Biochemical studies of erythropoietin and erythropoietin receptors". Thesis, Queen's University Belfast, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334533.
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McNamee, P. T. "A study of erythropoietin and factors regulating erythropoiesis in chronic renal failure". Thesis, Queen's University Belfast, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374226.
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Cervellini, Ilaria. "Neuroprotection by erythropoietin". Thesis, University of Brighton, 2012. https://research.brighton.ac.uk/en/studentTheses/1075c7e4-6f7d-4f53-b83e-42671edac8ca.
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Erythropoietin (EPO) is an erythropoietic cytokine that is also neuroprotective in vitro and in vivo. Neither the mechanism of action of EPO in neuroprotectio, nor the receptor involved is completely known. In fact, EPO regulates erythropoiesis by the homodimeric EPO receptor (EPOR)2. Variants of EPO, not binding (EPOR)2, are still neuroprotective, therefore another receptor may mediate this effect. In vivo, EPO is anti-inflammatory in several models of disease but, to date, a direct anti- inflammatory effect in vitro has not been clearly found. The focus of this thesis work was a twofold. Firstly, a direct anti-inflammatory effect of EPO was investigated in vitro. It was confirmed that EPO did not have any effect on production of cytokines induced by LPS. In addition, EPO did not reduce cytokines induced by alarmins and other inflammatory stimuli. EPO did not inhibit the pro-inflammatory receptor TREM-1. Finally, EPO did not act as anti-inflammatory by mobilization of endothelial precursor cells in vivo. The second focus of this thesis work was the study of a possible role of EPO on myelination by analysing the induction of myelin genes during differentiation of an oligodendrocyte cell line. EPO upregulated myelin gene expression (MaG and MBP), as studied by qPCR and Western Blot. EPOR was required for the effect of EPO, observed only in cells overexpressing EPOR. EPO induced high levels of the early growth response gene EGR2 that was however not involved in myelin gene induction. Finally, EPO was unable to induce myelin genes in an in vivo model of demyelination induced by cuprizone, neither at the peak of demyelination (3 and 5 weeks) nor during the recovery phase. Greater understanding of effects and mechanisms of action of EPO in the CNS would be useful to find new therapies promoting repair, for instance in diseases like MS in which no drug is available for that purpose.
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Krosl, Jana. "The role of erythropoietin and erythropoietin receptor in regulation of hemopoiesis". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq25081.pdf.
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Zhang, Yingxin. "Symmetric signaling by an asymmetric 1 erythropoietin : 2 erythropoietin receptor complex". Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/45211.
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Thesis (M. Eng.)--Massachusetts Institute of Technology, Biological Engineering Division, 2008.Includes bibliographical references (p. 43-46).
One erythropoietin molecule binds asymmetrically to two identical receptor monomers via erythropoietin site 1 and site 2, although it is unclear how asymmetry affects receptor activation and signaling. Here we report the computational design and experimental validation of two mutant erythropoietin receptors: one that binds only to erythropoietin site 1 but not site 2, and one that binds only to site 2 but not site 1. Expression of either mutant receptor alone in Ba/F3 cells cannot elicit a signal in response to erythropoietin, but when co-expressed, there is a proliferative response and activation of the JAK2 Stat5 signaling pathway. A truncated erythropoietin receptor with only one cytosolic tyrosine (Y343), on only one receptor monomer is sufficient for signaling in response to erythropoietin, regardless of the monomer on which it is located. The same results apply to having only one conserved juxtamembrane hydrophobic L253 or W258 residue, essential for JAK2 activation, in the full-length receptor dimer. We conclude that despite asymmetry in the ligand-receptor dimer interaction, both sides are competent for signaling, and we suggest that the receptors signal equally.
by Yingxin Zhang.
M.Eng.
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Yu, S. R. "Cytoprotective mechanisms of erythropoietin and erythropoietin derivatives in peripheral arterial disease". Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1458006/.
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A third of patients with critical limb ischaemia (CLI) eventually require amputation. Inconsistencies between successful revascularisation and functional outcomes exist, and underlying musculopathy in CLI patients has been identified. Erythropoietin (EPO) has tissue-protective effects in response to ischaemic injury, but its clinical use is often precluded by thromboembolic side effects. Non-haematopoietic EPO-derivatives have been designed to retain only tissueprotective functions of EPO. We hypothesised that ARA-290 (EPO-derivative) may have tissue-protective potential that could represent a novel therapeutic adjunct in patients with CLI. The effect of EPO and ARA-290 in mediating cytoprotection in an in vitro simulated ischaemia model of skeletal muscle was assessed firstly in the immortalised murine C2C12 myoblast cell line and subsequently in skeletal myoblasts isolated from CLI and control donors. In human and murine cells, simulated ischaemia alone demonstrated a detrimental effect on cell function and survival. Addition of EPO or ARA-290 demonstrated significant improvements in function and survival and utilised JAK2/STAT3, PI3k/Akt and NF!B signalling molecules. Isolation of human skeletal myoblasts from CLI patients has not previously been described. Comparison of CLI and control myoblasts elucidated significant differences in their function and survival under both normoxic and simulated ischaemic conditions. CLI myoblasts and myotubes exhibited increased proliferative capacity but reduced migratory and contractile function and importantly a reduced susceptibility to a second ischaemic-insult compared with control myoblasts and myotubes. Evaluation of several variations in the hindlimb ischaemia model allowed the creation of a model which closely recapitulated the muscular pathology observed in human CLI patients. ARA-290 demonstrated improved functional, histological and perfusion outcomes compared to EPO or vehicle-control treated animals. These studies demonstrate the potential of ARA-290 to protect tissues and cells from ischaemic-injury and encourages the development of novel pharmacological therapies for use in patients with “no option” CLI or severe functional deficit.
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Chang, Kai-Hsin 1974. "Erythropoietin, erythropoiesis, and malarial anemia : the mechanisms and implications of insufficient erythropoiesis during murine blood-stage malaria". Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84490.
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Severe anemia is a major life-threatening complication of malaria. Inappropriately low reticulocytosis in malaria patients with anemia suggests insufficient erythropoiesis, of which the mechanisms and implications are not clear. The principle growth factor that promotes erythropoiesis is erythropoietin (Epo). Studies determining the serum level of Epo in malaria infected patients have been inconclusive. Furthermore, the role of Epo and the erythropoietic response to Epo stimulation during malaria have never been examined. The purpose of the experiments performed in this thesis was, thus, to investigate the role of Epo and erythropoiesis in relation to anemia during blood-stage malaria using the murine model of Plasmodium chabaudi AS. A murine Epo specific ELISA, which was determined to be less biased by the presence of other cytokines in the samples as compared to the conventional Epo bioassay, was first developed to facilitate the research. The kinetics of Epo production in the kidney and the levels in the serum were characterized. It was demonstrated that Epo production during blood-stage malaria is mainly regulated by the degree of anemia and that renal cytokines may have only a minor effect on this response. Next, the roles of Epo and erythropoiesis during blood-stage malaria were investigated by neutralization of endogenous Epo or by administration of exogenous Epo. Timely onset of Epo-induced reticulocytosis was shown to be important for the alleviation of malarial anemia and survival. However, reticulocytosis in response to Epo stimulation is severely suppressed by infection with malaria. Dissection of the upstream events of erythropoiesis demonstrated that blood-stage malaria compromises the generation of reticulocytes by suppressing the proliferation, differentiation, and maturation of erythroid-lineage cells at various stages of erythroid development. Taken together, our data provide important insights for understanding the patho
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Rolfes, Simone [Verfasser]. "Einfluss von Erythropoietin und Erythropoietin-Isoformen auf die murine Neurogenese / Simone Rolfes". Berlin : Freie Universität Berlin, 2016. http://d-nb.info/108193543X/34.
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Barbeau, Paule. "Markers of the erythropoietin, erythropoietin receptor and RAD genes and cardiorespiratory endurance". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq25376.pdf.
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Lipšic, Erik. "Erythropoietin in cardiac ischemia". [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2006. http://irs.ub.rug.nl/ppn/293076030.
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Sharples, Edward John. "Pleiotropic effects of erythropoietin". Thesis, Queen Mary, University of London, 2011. http://qmro.qmul.ac.uk/xmlui/handle/123456789/2351.
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The haematopoietic growth factor Erythropoietin (EPO) is essential for the survival of erythroid progenitors to maturation and differentiation. It has been recognised that the EPO signalling pathway is also present in other tissues including the brain and vasculature, and is integral to the physiological response to ischaemia. Exogenous EPO was found to improve the outcome in animal models of stroke. The primary aim of this thesis was to examine whether erythropoietin was protective in a model of acute kidney injury, and to determine the mechanism by which EPO exerted this effect. In vitro experiments using HK-2 cells, a human tubular epithelial cell line, showed that EPO induced dose-dependent changes in cell number, and activated a number of intra-cellular signalling pathways. EPO reduced apoptotic cell death induced by nutrient starvation through the expression of anti-apoptotic proteins. A short-term model of ischaemia reperfusion was used to determine that EPO reduced the development of acute kidney injury, with a reduction in caspase activity and apoptosis. Longer models of ischaemia were then performed to confirm these findings, and showed that a pre-conditioning regime before the onset of the insult was also effective. In order to examine the mechanism of action, EPO was used in a model of cisplatin-induced kidney injury. EPO reduced apoptosis and caspase activation through the maintenance of mitochondrial membrane potential, inhibition of stress kinase signalling, and expression of XIAP and Bcl-XL. EPO also reduced the induction of oxidative stress and PARP-1 activity. EPO was then given to animals exposed to cisplatin and confirmed the finding that pretreatment with EPO significantly reduced cisplatin nephrotoxicity. Finally, EPO was used in a model of myocardial infarction and heart cells in culture to confirm that EPO plays a significant physiological role in cellular protection in multiple tissues.
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Langer, Juliane [Verfasser]. "Untersuchungen zur Erythropoietin-Konzentration im Urin Frühgeborener nach Applikation von rekombinantem Erythropoietin / Juliane Langer". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2012. http://d-nb.info/1028496087/34.
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Richardson, Dominique. "Synthesis of neo-glycosylated human erythropoietin and investigation into interaction with the erythropoietin receptor". Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/synthesis-of-neoglycosylated-human-erythropoietin-and-investigation-into-interaction-with-the-erythropoietin-receptor(6c7e44b5-e7f4-46b7-beb0-cd7f8b15b757).html.
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Erythropoietin (EPO) is the glycoprotein hormone responsible for regulating the production of erythrocytes. EPO also plays a cytoprotective role in a variety of tissues, including the brain and heart, by preventing apoptosis of healthy cells after ischemic injury (tissue protection). Recombinant human EPO (rhEPO) used clinically to treat anaemia is unsuitable for administration as a tissue protective agent due to the adverse side effects associated with overstimulation of erythropoiesis. As such, there have been a number of attempts to develop a tissue protective EPO derivative by eliminating erythropoietic function. Reported here is the synthesis of neo-glycosylated human erythropoietin and investigation into the effect this modification has on the interaction of EPO with its erythropoietic receptor (EPOR)2. In order to develop a non-erythropoietic EPO derivative, cysteine residues were introduced into the EPO sequence to act as chemical modification sites. EPO variants were then glycosylated at the cysteine residues using a one-step synthesis with alpha-mannosyl iodoacetamide before analysis by ELISA. Residues located within the two binding sites of EPO were targeted for mutation, and a total of 13 EPO variants were generated and expressed from E. coli. Upon expression and purification, EPO cysteine variants were glycosylated with alpha-mannosyl iodoacetamide. Reaction of single EPO variants yielded a mixture of unmodified and mono-glycosylated EPO species. Reaction of the double cysteine EPO variants yielded a mixture of three species; the unmodified EPO, the mono-glycosylated EPO and the di-glycosylated EPO. To determine the effect of this glycosylation on the EPO-(EPOR)2 interactions, an ELISA based assay was developed. Initially, all EPO variants were screened by ELISA for WT-like binding to the (EPOR)2. Of the 13 variants screened only the K45C+K97C EPO variant was used in the proof-of-concept study. Comparison of the WT EPO before and after reaction with the alpha-mannosyl iodoacetamide on the ELISA showed no inhibition of the EPO-(EPOR)2 interactions while comparison of the K45C+K97C EPO before and after reaction showed a statistically significant difference in the EPO-(EPOR)2 binding. This outcome indicates that it is possible to inhibit the EPO-(EPOR)2 binding by introducing non-natural glycosylation sites in to the EPO sequence.
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Zhang, Ji. "Mechanisms of erythroid proliferation and differentiation analysis of the role of erythropoietin receptor in the friend virus model /". View the abstract Download the full-text PDF version (on campus access only), 2008. http://etd.utmem.edu/ABSTRACTS/2008-025-JiZhang-index.html.
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Thesis (Ph.D. )--University of Tennessee Health Science Center, 2008.Title from title page screen (viewed on October 7, 2008 ). Research advisor: Paul A. Ney, M.D. Document formatted into pages (xi, 122 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 78-110).
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Maxwell, P. H. "Regulation of the erythropoietin gene". Thesis, University of Oxford, 1994. http://ora.ox.ac.uk/objects/uuid:86a152eb-cfc8-4812-935e-c89ab48acee3.
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Erythropoietin (Epo) is a circulating hormone which regulates red blood cell production, and hence oxygen-carrying capacity. Three striking features of Epo gene expression are that it shows high level induction in response to hypoxia, that it is tightly tissue-restricted and that it is deficient in most forms of renal damage. Each of these aspects has been investigated in this thesis. Chapter 3 concerns the hypoxic-sensing system which induces Epo gene expression via an enhancer element in cultured hepatoma cells. Transient transfection was used to examine a range of cell-lines, which did not produce Epo, for the presence of this oxygen-sensing system. It was demonstrated that such a system is widespread in mammalian cells. It is probable that it is involved in regulating the expression of other genes in response to hypoxia. This widespread oxygen-sensing mechanism contrasts with the tightly tissue-restricted expression of the Epo gene. Transgenic experiments described in Chapters 4 and 5 provide data concerning the DNA sequences involved in this tissue specificity. Sequence from the mouse Epo locus was then used to direct expression of a marker protein, SV40 T antigen, to Epo-expressing cells. This led to identification of the Epo-producing cells in the kidney (Chapter 5) and liver (Chapter 6). In both organs a fibroblast-like population expresses the gene; the Ito cells in the liver and the Type 1 interstitial cells in the kidney. In the liver hepatocytes also produce Epo. Further studies of Epo gene expression would be facilitated by the availability of Epo-producing cell lines. SV40 T antigen is a viral oncogene, and expression of this protein was used as a proliferative stimulus in vivo. The effects of this, and attempts to isolate these cells form the subject of Chapter 7. Chapter 7 also describes experiments in which renal injury was combined with visualisation of individual Epo-producing cells. A homologous recombination at the Epo locus resulted in an allele which expressed the hormone at a greatly reduced level. The phenotype of animals homozygous for this allele is described in Chapter 8. Experiments designed to produce further modification of the Epo locus by this method, and to assess its utility in modifying the mouse genome are also described.
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Stewart, J. P. "Erythropoietin-induced genes and the erythropoietin receptor : their possible role in the pathogenesis of multiple myeloma". Thesis, Queen's University Belfast, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396562.
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Görden, Stephan [Verfasser]. "Untersuchungen zur Erythropoietin- und Erythropoietin-Rezeptor-Expression nach experimenteller spinaler Kontusion in der Ratte / Stephan Görden". Kiel : Universitätsbibliothek Kiel, 2018. http://d-nb.info/1164012509/34.
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McKeveney, Paul J. "Characterisation of novel erythropoietin-responsive genes". Thesis, Queen's University Belfast, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301746.
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Murthy, Sudish C. "An examination of in vitro erythropoiesis by utilizing agents that mimic the in vitro activity of erythropoietin". Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26503.
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The major in vivo hormonal regulator of terminal erythropoiesis is erythropoietin (Ep). This 38,000 dalton acidic glycoprotein has been shown to stimulate the formation of hemoglobinizing erythroblasts. Two in vitro assays designed to measure Ep bioactivity were utilized to determine if other agents could mimic Ep activity in vitro. It was hoped that this approach might yield insights into the mechanism of action of Ep. Several agents have now been identified, and two, dimethyl sulfoxide (DMSO) and sodium orthovanadate had previously been shown (in other systems) to stimulate membrane phosphorylation changes. Accordingly, Ep, DMSO and sodium orthovanadate were assayed with Ƴ-³²P-ATP and plasma membranes purified from Ep-responsive cells to determine if each could induce significant phosphorylation changes as assessed by sodium dodecyl sulfate polyacrylamide gel electrophoresis and autoradiography. It was found that while both sodium orthovanadate and DMSO effected profound phosphorylation alterations, Ep did not elicit any detectable phosphorylation changes. Specifically, vanadate caused a generalized increase in membrane base-stable phosphoproteins, and DMSO reproducibly stimulated the base resistant phosphorylation of a 35 Kd membrane-associated protein. It is reasonable to postulate that the latter phosphorylation event might be responsible for the stimulatory activity of DMSO on terminally differentiating erythroid cells.
To understand whether Ep and Ep-mimicking agents were operative on the same target cell population, homogeneous, virally-infected, erythroblasts were cultured in vitro and assayed for ³H-thymidine incorporation in the presence of each agent at various intervals during erythroid cell differentiation. It was found that Ep greatly stimulated very early, as well as differentiated, erythroblasts to proliferate, while four different Ep-mimicking agents could only effect thymidine incorporation into a more mature erythroid population. From this work it is conceivable that Ep-mimicking agents stimulate in vitro erythropoiesis through specific membrane phosphorylation changes and function primarily on late erythroblasts, while the mechanism of action of Ep on primitive and late erythroblasts remains unresolved.Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Mattar, Julia Eva. "Einfluss von Adenosin-2'-3'-Dialdehyd auf das Methylierungspotential und die Genexpression in HepG2-Zellen unter normoxischen Bedingungen". [S.l. : s.n.], 2004.
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Wirtz, Joris Jeroen Johannes Maria. "Hemodynamic and hemostatic effects of erythropoietin therapy". Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1993. http://arno.unimaas.nl/show.cgi?fid=5887.
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Smith, Katie. "The impact of erythropoietin on uraemic cardiomyopathy". Thesis, University of Hull, 2009. http://hydra.hull.ac.uk/resources/hull:2679.
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Cardiovascular complications are the leading cause of death in patients with chronic kidney disease (CKD). The uraemic heart is characterised by cellular and structural remodelling, including left ventricular hypertrophy LVH), which contribute to heart failure. Erythropoietin (EPO) has evolutionised the treatment of the anaemia associated with CKD. The discovery that the EPO receptor is also expressed on cardiomyocytes highlights a role of EPO beyond haematopoiesis. However, little is known on the cellular impact of EPO on the uraemic heart. The aim of this study was to determine the effect of EPO administration on uraemic cardiomyopathy.Uraemia was induced surgically in male Sprague-Dawley rats via a subtotal nephrectomy and animals retained for 3, 6, 9 or 12 weeks post-surgery. EPO was administered subcutaneously twice a week for 2 weeks prior to sacrifice at a dose of 30 μg/Kg. Cardiac function was assessed in vitro in the perfused heart and in vivo using an arterial pressure catheter. Cardiac metabolism was analysed using 13C NMR along with the activity and protein expression of key metabolic enzymes. In a separate set of experiments, mitochondrial function was determined in vitro using an oxygen electrode. To determine the extent of cardiac fibrosis, collagen was stained using picro-sirius red in frozen sections.Kidney dysfunction was observed from 3 weeks post-surgery as evident by significantly raised serum creatinine and urea, and development of anaemia. LVH was present at 6 and 12 weeks post-induction of uraemia, however in vitro and in vivo cardiac function was preserved,highlighting a compensatory phase. EPO did not impact on renal function, however, EPO significantly improved haematocrit and induced regression of LVH in uraemic animals at 12 weeks. In addition to preserved cardiac function, myocardial mitochondrial respiration was not modified by uraemia and unaffected by EPO administration. There was a decrease in palmitate utilisation in uraemic hearts compared to controls at 6 weeks post-surgery despite the unchanged activities of key metabolic enzymes including citrate synthase, medium chain acyl-CoA dehydrogenase and pyruvate dehydrogenase activity. Furthermore, the protein expression of CD36 and PPARα was the same in uraemic and control hearts. At 12 weeks post-surgery, uraemic animals exhibited significantly increased collagen within the heart compared to controls, highlighting cardiac fibrosis.In summary, by 12 weeks post-induction of uraemia, animals exhibited impaired kidney dysfunction, LVH, metabolic remodelling and cardiac fibrosis with preserved cardiac and mitochondrial function. Further work is required to determine whether the structural and metabolic remodelling which accompany uraemic cardiomyopathy would lead to a deterioration in cardiac function with prolonged uraemia.
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Tam, Robert C. "Aspects of the physiology of erythropoietin secretion". Thesis, Open University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278491.
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Kobayashi, Toshihiro. "Production of Erythropoietin in the Reproductive Organs". Kyoto University, 2003. http://hdl.handle.net/2433/148962.
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Kyoto University (京都大学)0048
新制・課程博士
博士(農学)
甲第10233号
農博第1305号
新制||農||862(附属図書館)
学位論文||H15||N3754(農学部図書室)
UT51-2003-H654
京都大学大学院農学研究科応用生命科学専攻
(主査)教授 永尾 雅哉, 教授 伏木 亨, 教授 吉川 正明
学位規則第4条第1項該当
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Rosenlöf, Katarina. "Erythropoietin receptor and comparison with renin substrate /". Hki : Societas scientiarum Fennica : Academic Bookstore [distr.], 1987. http://catalog.hathitrust.org/api/volumes/oclc/57854069.html.
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Diss. -- Helsingin yliopisto.Tiivistelmä ja 5 erip. - Tiivistelmä ilm. myös erillisenä. - Nimiösivulla myös: From the Minerva Foundation Institute for Medical Research, Unit of Clinical Physiology, and the Fourth Department of Medicine, University of Helsinki.
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Breggia, Anne C. "The JAK2/Y343/STAT 5 Signaling Axis is Required for Erythropoietin - Mediated Protection against Ischemic Injury in Renal Tubular Epithelial Cells". Fogler Library, University of Maine, 2008. http://www.library.umaine.edu/theses/pdf/BreggiaAC2008.pdf.
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Paul, Christina. "Expression und Wirkung von Erythropoietin ß bei Astrozyten unter normoxischen und hypoxischen Bedingungen". [S.l. : s.n.], 2007.
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Mayuzumi, Daisuke. "Role of receptor ubiquitination in erythropoietin receptor signaling". Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/854.
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Erythropietin (Epo), acting through its receptor (EpoR), is an essential hemotopietic growth factor that regulates the proliferation, differentiation, and survival of erythroid progenitor cells. Perturbations of Epo/EpoR function cause myeloproliferative disease, such as erythrocytosis, or myelodeficient disease, such as anemia. Therefore, defining the mechanisms by which Epo/EpoR control proliferation and differentiation of erythroid cell lineages attracts interest. Ubiquitin-dependent internalization and degradation is a common regulatory mechanisms affecting signaling from a variety of receptors. Although EpoR has been found to be ubiquitinated, the function of EpoR ubiquitination in the regulation of Epo signaling remains unclear. Therefore, the primary goal of this study was to define the role of EpoR ubiquitination in regulating Epo signaling activities and erythroid cell growth. We showed that EpoR was ubiquitinated in response to ligand stimulation, and that loss of EpoR ubiquitination reduced signaling activity and biological responses to low dosages of Epo. We also identified two EpoR lysines that were the primary targets for ubiquitination, and showed that either ubiquitination site supported the enhanced activities of wild-type-EpoR. Ubiquitination of EpoR was also associated with a change in the endocytic pathway mediating internalization of EpoR. Specifically, constitutive internalization of non-ubiquitinated EpoR was found to depend on dynamin activity, while internalization of ubiquitinated EpoR was dynamin-independent but could be inhibited by disrupting lipid raft microdomains in the plasma membrane. Interestingly, inhibiting internalization of ubiquitinated EpoR (by disrupting lipid rafts) specifically reduced signaling from ubiquitinated receptors without affecting signaling from non-ubiquitinated receptors. Conversely, reducing internalization of non-ubiquitinated EpoR (by inhibiting dynamin) reduced its signaling activity without affecting signaling from ubiquitinated receptors. This strong correlation between EpoR internalization and signaling activity suggests a novel regulatory mechanism in which internalization of EpoR facilitates its signaling activity. In this regard, Epo-induced ubiquitination of EpoR promotes more efficient internalization of ligand-activated receptor and may contribute to enhanced responsiveness to low concentrations of Epo.
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Lau, Monique [Verfasser]. "Wechselwirkungen der Transkriptionsmodulatoren Wt1, Gata4 und Retinsäure mit dem Erythropoietin/Erythropoietin-Rezeptor-System des embryonalen Herzens der Maus / Monique Lau". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2021. http://d-nb.info/1234985071/34.
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Pham, Michael N. "Erythropoietin Stimulation of Mitochondrial Protein Content - A Potential Mechanism through Direct Binding of Erythropoietin Receptor and AMP-Activated Protein Kinase". Diss., The University of Arizona, 2014. http://hdl.handle.net/10150/321354.
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Proliferating cells have unique metabolic requirements beyond those of quiescent cells. Specifically, blood forming hematopoietic stem cells, during periods of severe blood loss, switch from a quiescent glycolytic state to a state dependent on mitochondrial metabolism during differentiation and proliferation. This dissertation attempts to define some of the signaling details of this switch by using erythropoietin receptor signaling as a model. In cytokine-dependent Ba/F3 cell line expressing the receptor for erythropoietin (EpoR) (Ba/F3-EpoR), chemical inhibition of mitochondrial function by rotenone decreases in erythropoietin(Epo)-stimulated proliferation. This observation led to the examination of whether Epo could stimulate mitochondrial function. To further assess the role of mitochondria in cell proliferation and the metabolic functions of Epo, levels of oxidative phosphorylation markers and signaling molecules important for mitochondrial biogenesis were measured. Western blotting scans showed increased protein levels of cytochrome oxidase subunit IV (CoxIV) and Complex III core protein 2 following 24 hours of Epo treatment. Interestingly, inhibition of Janus Kinase 2 (Jak2), the tyrosine kinase associated with Epo receptor, by AG490 elicited a similar decrease in CoxIV to Epo withdrawal even in the presence of Epo. In addition, Epo increased the levels of the mitochondrial biogenesis regulator AMP-activated protein kinase α (AMPKα) in a Jak2-dependent manner within Ba/F3 cells. Both total and phosphorylated (activated) AMPKα were increased following Epo stimulation. Treatment with the AMPK inhibitor Compound C decreased Epo stimulation of CoxIV, suggesting a linear signaling cascade from Jak2 to mitochondrial biogenesis through AMPKα. Examining potential mechanisms, direct binding of AMPKα to (EpoR) and Jak2 were observed through immunoprecipitations of transfected lysates in a manner exclusive to AMPK regulator subunits β and γ. Furthermore AMPKα was found to be tyrosine phosphorylated in an Epo and Jak2 dependent manner. Taken together, data in this dissertation suggests a role for Epo in regulating mitochondrial biogenesis in cytokine dependent cells through a potential mechanism of forming a signaling complex between EpoR, Jak2, and AMPKα. This signaling complex may provide intersection between Epo's signaling in cell proliferation and metabolism through AMPKα.
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Sauer, Katja. "Inhibition der Müllerzellschwellung durch Erythropoietin unter hypotonen Bedingungen". Doctoral thesis, Universitätsbibliothek Leipzig, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-105242.
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The volume homeostasis of retinal glial cells is mediated by an autocrine purinergic mechanism of ion channel opening which is activated in response to a decrease in the extracellular osmolarity. Here, I show that erythropoietin (EPO) prevents the osmotic swelling of glial somata in retinal slices from control and diabetic rats, with a half-maximal effect at approximately 0.01 nM. The downstream signaling evoked by EPO includes a release of vascular endothelial growth factor from the cells which was blocked by Janus kinase and extracellular signal-regulated kinases (ERK)1/2 inhibitors. Transactivation of kinase insert domain-containing receptor/fms-like tyrosine kinase 1 (KDR/flk-1) evokes a calcium-dependent, exocytotic release of glutamate, followed by activation of group I/II metabotropic glutamate receptors which results in calcium-independent release of ATP and adenosine from the cells. The final step in this cascade is the activation of adenosine A(1) receptors which results in protein kinase A- and phosphoinositide 3-kinase-mediated opening of potassium and chloride channels. EPO receptor protein was immunohistochemically localized to the inner retina and photoreceptor inner segments. In isolated glial cells, EPO receptor protein is selectively localized to fibers which traverse the inner nuclear layer in situ. Inhibition of glial swelling might contribute to the neuroprotective action of EPO in the retina under pathological conditions.
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Hardy, Sinead M. "Nanoparticles versus microarrays in the detection of erythropoietin". Thesis, University of East Anglia, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502039.
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Horseracing is a huge industry both nationally and internationally. With large financial rewards now available at some meetings the pressure to excel has grown and as a result the desire to win has led some racehorse owners to resort to the use of performance enhancing drugs. Rumours concerning the abuse of recombinant human erythropoietin (rHuEPO) in thoroughbred horseracing have been circulating since it became readily available in the late 1980s. While there are a number of commercially available EPO enzyme-linked immunosorbent assays (ELlSAs) to detect the administration of rHuEPO to horses, these kits are all restricted in their success due to the limited amount of time EPO remains in the horse's circulation. It is thought that the horse's immune system recognises the rHuEPO as a foreign protein and produces antibodies against it. This research aims to exploit this phenomenon to develop a new sensing system for the detection of rHuEPO antibodies resulting from rHuEPO administration. This research was divided into two parts. In the first section, a simple colorimetric assay based on the aggregation of gold nanoparticles for the detection of the antibodies produced as a result of rHuEPO abuse was developed. Various forms of rHuEPO have been attached to gold nanoparticles via linkage molecules to develop colorimetric assays based on the aggregation of protein-modified gold nanoparticles and its corresponding antibody. The 17 nm protein-stabilised nanoparticles are ruby red in colour. The sensing system was tested with the anti-HuEPO antibody. Upon addition of this antibody, aggregation occurred, with a subsequent change in colour from red to purple due to a red-shift in the surface plasmon absorption band, which was monitored by UV/visible spectrophotometry. For each variant of rHuEPO, the theoretical limit of detection (LOD) was established and kinetic studies (time to complete the aggregation reaction) were investigated.
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Maxwell, Alexander Peter. "Studies of the biology and pharmacology of erythropoietin". Thesis, Queen's University Belfast, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335933.
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Taylor, Timothy Nicholas. "Immunochemical studies of erythropoietin in chronic renal failure". Thesis, Queen's University Belfast, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356918.
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Daghman, Nureddin A. "A study of the factors regulating erythropoietin production". Thesis, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337043.
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Emanuelsson, Ida, Anna-Karin Jansson i Katarina Risö. "Characterising of chromatography gels for purification of erythropoietin". Thesis, Högskolan i Borås, Institutionen Ingenjörshögskolan, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:hb:diva-19097.
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Erythropoietin is a human natural hormone which task is to regulate the amount of red blood cells in the body. At Centro de Inmunología Molecular, situated in Havana, erythropoietin is produced by recombinant DNA-technique. The protein is purified through several chromatography steps. Among other things, Centro de Inmunología Molecular uses affinity chromatography and ion exchange chromatography. To both of these chromatographic methods, gel is used as stationary phase. The aim of this study was to investigate and determine parameters for characterising of two gels, this because Centro de Inmunología Molecular have to exchange the gels. The reason for the gel exchange is that the currently used gels will not be manufactured any more. The gel used in the affinity chromatography is Chelating Sepharose Fast Flow and the gel used in the ion exchange chromatography is Q Sepharose Fast Flow. For both of this gels kinetic parameters and isotherm parameters were determined by experiments. The isotherm parameters qmax and Kd were calculated from an adsorption isotherm. To be able to calculate qmax and Kd for both Q Sepharose Fast Flow gel and Chelating Sepharose Fast Flow gel different experiments were made. A kinetic adsorption and an isotherm adsorption were made on each gel. The kinetic adsorption was made in due to find out how long the two different processes were supposed to run and to understand which part of the mass transfer that is controlling the rate. There is no use to let the process to be in progress any longer than until the adsorption ceases. For the Q Sepharose Fast Flow gel this was after 200 seconds. The adsorption with the Chelating Sepharose Fast Flow gel never ceased completely, but after 1000 seconds the adsorption was so slow that it would be no use to continue the process. If the processes continue after the calculated times only money, hours and recourses will be wasted. The data that were achieved was plotted in two different isotherm adsorption models both the Freundlich- and the Langmuir model, this to determine which model that had the best fit. One could see that the Q Sepharose Fast Flow gel was following the model of Langmuir better and because of this the Langmuir equation was used to calculate qmax and Kd. The qmax for the Q Sepharose Fast Flow gel agreed a lot with the value that Centro de Inmunología Molecular had assumed. When it came to the Chelating Sepharose Fast Flow gel, the same kind of plotting was made. But one could see that this time the data was following the model of Freundlich much better. Therefore a calculation of the desired qmax was impossible. Only the value of Kd was calculated. Because the company Centro de Inmunología Molecular still needed the value of qmax an assumption that the gel was following the model of Langmuir was made. qmax was calculated but without any satisfied results. The programs Excel, Statgraphic and Matlab have been used in all calculations.Uppsatsnivå: C
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Bullard, Anthony John. "The role of erythropoietin in ischaemia/reperfusion injury". Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445332/.
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Background - Ischaemia/reperfusion accounts for a large proportion of fatalities in the developed world. Even if death is avoided, the patient suffers a deterioration in their quality of life. Erytriropoietin (EPO) has been examined in clinical studies investigating its effect in anaemic chronic heart failure patients with any positive effect attributed to the correction of anaemia. Given the recent discovery of the EPO receptor on the myocyte surface, this thesis examined whether EPO could have a direct effect on the myocardium and limit ischaeinia/reperfUsion injury and the mechanism by which any protection occurs. Methods and results - Using an isolated perfused rat model of ischaemia/reperfusion, we demonstrated that EPO could mimic preconditioning in a P1-3-Kinase (PI3K)- dependent manner. Adrninistration of EPO at reperfusion limited infarct size by activation eNOS and could be abolished by inhibitors of NOS, PI3K and ERK 1/2. This thesis also showed that EPO could delay mitochondrial permeability transition pore opening (mPTP) in an oxidative stress myocyte model of mPTP opening, an effect that was suppressed by inhibitors of NOS and PBK. A 3 week treatment of EPO reduced injury in a NOS-dependent manner that was independent of haematocrit. Finally this thesis demonstrated that administration of EPO as late as 30 minutes after commencement of reperfusion could still reduce infarct size. Conclusion - This thesis demonstrated that EPO can be used in a variety of settings to elicit a protective effect against ischaemia/reperfusion injury. This variety of effective time points promises an important future role for EPO in the treatment of ischaemic heart disease.
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O'Leary, Olivia Eileen. "The therapeutic potential of erythropoietin for ischaemic retinopathies". Thesis, Queen's University Belfast, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.696156.
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Ischaemic retinopathies are characterised by dysfunction and degeneration of retinal vascular networks, leading to the compensatory development of sight-threatening vasoproliferative pathology. The scope for treating these diseases is limited and, as such, they continue to represent a significant cause of visual impairment globally. Erythropoietin (EPO) has demonstrated tissue-protective abilities in ischaemic injury, settings, but its clinical use is precluded by concerns that it could lead to thromboembolic events or exacerbate pathological retinal angiogenesis. ARA 290, a peptide based on the B helix of EPO, is non-erythropoietic whilst maintaining tissue-protective properties. We hypothesised that ARA 290 could be used as a novel therapeutic to target multiple facets of ischaemic retinopathies. To test this hypothesis, we investigated the potential of ARA 290 for use either as a stand-alone pharmacotherapy to prevent vasodegeneration, or to stimulate microvascular repair, in conjunction with endothelial colony forming cells (ECFCs), a vasculogenic endothelial progenitor cell subpopulation. The vasoprotective potential of ARA 290 in the context of retinopathy of prematurity was investigated in a preventive paradigm, using a murine model of hyperoxia-induced retinal vasodegeneration. In this context, ARA 290 was found to be unsuitable as a vasoprotective monotherapy. In the STZ-induced diabetic mouse ARA 290 administered three times weekly for the duration of hyperglycaemia was associated with preservation of retinal function and reduction in retinal inflammation, as evidenced by reduced Müller gliosis and the reduced gene expression of a panel of inflammatory markers. ECFCs were isolated from human umbilical cord blood monocytes cultured on collagen. In the murine oxygen-induced retinopathy (OIR) model of retinal ischaemia, vasorepair by ECFCs was enhanced in the presence of ARA 290. These studies provide important insight into the potential application of ARA 290 as a novel therapeutic for the ischaemic retina.
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Wallach, Iwona. "Transkriptionelle Regulation des Erythropoietin-Rezeptor-Gens im zentralen Nervensystem". Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2007. http://dx.doi.org/10.18452/15685.
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Derzeit wird die Anwendung von Erythropoietin (Epo) zur Neuroprotektion in präklinischen und klinischen Studien intensiv untersucht. Für die Neuroprotektion ist die Regulation des Erythropoietin-Rezeptors (EpoR) in neuronalen Zellen von hoher Relevanz. In dieser Arbeit wurden die transkriptionellen Mechanismen der EpoR-Regulation in humanen Neuroblastom-Zellen SH-SY5Y mit neuronalem Phänotyp untersucht. Da der hämatopoietische Transkriptionsfaktor GATA-1 die EpoR-Transkription in erythroiden Vorläuferzellen in Kooperation mit Sp1 stimuliert, wurde die Rolle der in neuronalen Vorläuferzellen exprimierten GATA-Transkriptionsfaktoren bei der EpoR-Expression untersucht. Es wurde eine in vitro Bindung von GATA-2, -3 und -4 an zwei Motive in der EpoR 5’-flankierenden Region (-274/-271; -47/-44) nachgewiesen. In Reportergen-Assays zeigten diese Genabschnitte eine bis zu 4,8-fache Aktivitätssteigerung bei Überexpression von GATA-2, -3 oder -4. Die endogene EpoR mRNA-Expression wurde dadurch aber nicht erhöht. Hypoxie (2% O2, 3 d) erhöhte die EpoR-Expression signifikant (1,8-fach, p < 0,01), wobei überexprimierte GATA-Transkriptionsfaktoren diesen Effekt nicht weiter steigerten. Die Gabe von Epo (5 U/ml, 3 d) hatte weder unter Normoxie noch unter Hypoxie einen Einfluss auf die EpoR-Expression. Die Promotoraktivität der Reporterkonstrukte wurde durch Mutation der GATA-Bindungsstellen nicht verändert, jedoch bei mutierter Sp1-Bindungsstelle inhibiert. Ein Fragment der 5’-flankierenden Region (-449/-285), das ein Cluster von Bindungsstellen für unterschiedliche Transkriptionsfaktoren enthält, zeigte die stärkste Promotoraktivität und rekrutierte offenbar die RNA-Polymerase II. In unserem Modell spielen die GATA-Faktoren keine direkte Rolle für die EpoR-Genregulation in neuronalen Vorläuferzellen. Die EpoR mRNA-Expression wird eher durch einen Komplex aus verschiedenen Transkriptionsfaktoren reguliert, der an eine 5’ des minimalen Promotors liegende DNA-Region zu binden scheint.Since the use of erythropoietin (Epo) as neuroprotective agent is currently intensively studied in preclinical and clinical trials, regulatory mechanisms of the erythropoietin receptor (EpoR) in neuronal cells are of particular interest. In this study, the transcriptional mechanisms of EpoR regulation were analyzed in human neuroblastoma-derived SH-SY5Y cells, which exhibit a neuronal phenotype. Considering that the hematopoietic transcription factor GATA-1 stimulates EpoR transcription in cooperation with Sp1 in erythroid progenitors, the role of other GATA family members expressed in neuronal precursor cells were studied. In vitro, GATA-2, -3 and -4 were found to bind to two consensus motifs within the EpoR 5’-flanking region (-274/-271 and -47/-44). In reporter gene assays, these regions showed an up to 4.8-fold induction if GATA-2, -3 or -4 were overexpressed. However, forced expression of GATA-2, -3 and -4 did not enhance endogenous EpoR mRNA expression. Under hypoxia (2% O2, 3 d), EpoR expression was significantly upregulated in SH-SY5Y cells (1.8-fold, p < 0.01), but not further increased by the additional overexpression of the GATA factors. Incubation of the SH-SY5Y cells with recombinant Epo (5 U/ml, 3 d) had no effect on the EpoR expression under normoxia or hypoxia. The promoter activities of the reporter constructs were not changed by mutations in the GATA sites, but abolished by mutations of Sp1 binding sites. A fragment (-449/-285) of the 5’-flanking region that contains a cluster of binding sites for various transcription factors showed strongest promoter activity and was obviously directing the recruitment of RNA polymerase II. We conclude that GATA factors do not play a major role in regulating EpoR expression in our model for neuronal precursor cells. EpoR mRNA expression is rather regulated by a complex of various transcription factors, which may bind to a region upstream of the minimal promoter.
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Glennie, Judith Lynn. "Is hypertension a determinant of erythropoietin requirements in hemodialysis?" Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0011/MQ41704.pdf.
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Di, Giovanni Jessica Louise. "Early second trimester amniotic fluid erythropoietin and pregnancy outcomes". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112615.
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The study objective was to determine whether early 2 nd trimester amniotic fluid (AF) erythropoietin (EPO) was associated with and predictive of (a) development of maternal gestational diabetes (GDM) and (b) the infant outcome parameters of (i) gestational age at birth (GAAB) assessed exclusively among spontaneous vaginal deliveries or (ii) birth weight (measured in grams and percentiles). Enzyme-linked-immunosorbent assay was used to determine the EPO concentration of 170 biobanked AF samples. Student's t-test revealed no difference between GDM and non-GDM subjects. AF EPO was not predictive of GAAB despite being significantly greater among preterm infants compared to post-term infants. In contrast, AF EPO was significantly higher among the smallest infants using both birth weight classification schemes. However, following inclusion of known covariates AF EPO was predictive of gram birth weight only. Early 2nd trimester AF EPO may emerge as a useful biomarker of fetal nutritional status and/or growth.
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Dobocan, Monica Crisanti. "Chaperonin 10: an endothelial-derived, erythropoietin- dependent differentiation factor". Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40690.
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Erythropoietin (EPO) stimulates endothelial cells to produce various factors that support the formation of erythroid cells. We identified by 2D electrophoresis/mass spectrometry one such factor as being chaperonin 10 (cpn10). Cpn10 was released in human umbilical vein endothelial cells (HUVEC) medium after EPO treatment; it decreased the proliferation of the erythroleukemic K562 cells, while stimulating differentiation in the erythroid TF-1 cells and skin fibroblasts. We analyzed the early events initiated by the addition of cpn10 in K562 and TF-1 cells and found significant changes in the phosphorylation levels of glycogen synthase kinase 3 (GSK-3) and cofilin-1. Further experiments using GSK-3 inhibitors in the presence or absence of cpn10 showed an alteration in the proliferation and differentiation patterns previously observed in TF-1 cells, suggesting a possible role for GSK-3 in cell differentiation as part of the signal transduction pathway triggered by cpn10. This is the first evidence linking cpn10 to erythropoiesis.L’érythropoïétine (EPO) stimule les cellules endothéliales à produire différents facteurs qui soutiennent la formation des érythrocytes. En effectuant une électrophorèse-2D / spectrométrie de masse, on a identifié la chapéronine10 (cpn10) comme étant un de ces facteurs. Cpn10 est secrétée par les cellules endothéliales HUVEC après un ajout d’EPO; elle diminue la prolifération des cellules érythroleucémiques K562 et elle stimule la différentiation des érythrocytes TF-1 et des fibroblastes. On a observé qu’une des actions immédiates initiées par cpn10 dans les cellules K562 et TF-1 était de changer significativement la phosphorylation de GSK-3 (glycogen synthase kinase 3) et cofilin-1. Des inhibiteurs de GSK-3 utilisés en présence de cpn10 ou seuls ont altéré le processus de prolifération et différentiation observés auparavant avec les cellules TF-1, en suggérant ainsi que GSK-3 puisse jouer un rôle dans la différentiation cellulaire déclenchée par cpn10. C’est la première fois qu’un lien est décrit entre cpn10 et l’érythropoïèse.
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Hamilton, Ross Waring. "The role of erythropoietin in protecting against diabetic retinopathy". Thesis, Queen's University Belfast, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.546354.
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Hufnagel, Maria [Verfasser]. "Genexpression von Erythropoietin durch Präkonditionierung des Zentralnervensystems / Maria Hufnagel". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1027497926/34.
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Zhang, Fenz. "Regulation of erythropoiesis in a murine model of chronic renal failure : the relative role of erythropoietin and insulin-like growth factor 1". Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=69733.
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Anemia is an almost invariable manifestation of chronic renal failure (CRF) and it often contributes substantially to the morbidity of the condition. In its uncomplicated form, this anemia is due primarily to reduced production of erythropoietin (EPO) by the diseased kidney. The present study was carried out in order to determine the relative role in the anemia secondary to CRF of EPO and insulin-like growth factor-1 (IGF-1), a recently recognized important regulatory factor of erythropoiesis in the normal physiological state.A mouse model of CRF was employed in this investigation. Six weeks after the surgical induction of renal failure, the mice were characterized in terms of biochemical and hematological parameters which included the response to a 3-week treatment with recombinant human EPO (r-HuEPO). Additionally the kidneys, liver and bone marrow were harvested for the determination of the mRNA expression of EPO and IGF-1 as assessed by the reverse transcription polymerase chain reaction followed by Southern blotting. Normal mice and mice rendered anemic by phlebotomy were included in all experiments. (Abstract shortened by UMI.)
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Colella, Pasqualina. "Use of erythropoietin derivatives for treatment of retinal degenerative diseases". Thesis, Open University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.548075.
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Held, Hanns-Christoph. "Die akute Wirkung von Erythropoietin am ischämischen Maus- und Schweineherz". Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-162319.
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Assaraf, Michael I. "The role of erythropoietin and its receptor in Alzheimer disease /". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81588.
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Background. Alzheimer Disease (AD) is a common progressive neurodegenerative disorder that results in impairment of memory, thinking and behavior (dementia). Objective. To delineate the patterns and extent of EpoR expression in the brains of patients with sporadic AD, Mild Cognitive Impairment (MCI; a frequent harbinger of AD) and normal elderly controls (NEC). Results. (A) Temporal cortex: Percentages of GFAP-positive astrocytes co-expressing EpoR were (i) significantly increased in AD and MCI vs. NEC (p<0.05) in layers II and III, (ii) increased in MCI, but not in AD, vs. NEC in layer I, and (iii) unrelated to diagnosis (p>0.05) in layers IV, V and VI and the subcortical white matter. (B) Hippocampus: Percentages of GFAP-positive astrocytes co-expressing EpoR were (i) significantly increased in AD and MCI vs. NEC (p<0.05) in the stratum oriens and pyramidal layer, (ii) increased in MCI, but not in AD, vs. NEC in the granular layer, stratum radiatum and dentate gyrus, and (iii) unrelated to diagnosis (p>0.05) in the molecular layer. Conclusions. (1) Up-regulation of astrocyte EpoR in certain cortical and hippocampal regions is an early event in the pathogenesis of sporadic AD. (2) Based on in vitro and whole animal studies, glial EpoR induction may confer protection against oxidative stress in the brains of patients with MCI and AD. (3) Clinical neuroprotection trials using Epo or its derivatives in MCI/AD may be warranted.
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Breen, Marie Elizabeth. "The erythropoietin receptor in TEL-AML1 positive acute lymphoblastic leukaemia". Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.579773.
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The TEL-AMLl fusion is the result of t(12;21) (p13;q22), the most frequent chromosomal translocation in childhood B-cell ALL. Recent studies have found a positive correlation with TEL-AMLl and EpoR expression. Three possible mechanisms of up-regulation were investigated in this study: Gene expression analysis, DNA methylation and microRNAs. Microarray analysis compared TEL-AMLl positive and negative gene expression profiles to identify differentially expressed genes. Genes with well known roles in haematopoiesis were also examined. GATA-2 showed a similar expression profile to EpoR, with a higher expression found in TEL-AMLl positive cells. Over-expression of GATA-2 increased EpoR expression further in TEL-AMLl positive cells providing evidence of a link between GATA-2 and EpoR expression in the presence of the fusion protein. DNA methylation analysis of EpoR and GATA-2 promoter regions showed a much higher level of methylation in TEL-AMLl negative cells. After treatment with a demethylating agent EpoR levels did not increase indicating EpoR expression was not epigenetically controlled. However, demethylation of GATA-2 increased expression in both TEL-AMLl positive and negative samples indicating a direct role for DNA methylation with GATA-2 expression. MicroRNAs are short non-coding RNA molecules with the ability to post-transcriptionally regulate genes by binding to the 3•UTR. Taqman microRNA arrays allowed simultaneous analysis of 667 commonly found microRNAs in both TEL-AMLl positive and negative cells. Arrays were analysed and compared with target prediction results to identify microRNAs that could target EpoR and GATA-2. Over-expression of miR-362 showed down-regulation of EpoR protein levels. Over-expression of miR-650 showed down-regulation of both GATA-2 and EpoR. Together these results support a theory of an "EpoR friendly" environment in TEL-AMLl positive cells to aid and promote EpoR expression. This includes an increase in GATA-2 and a decrease in DNA methylation and microRNA expression. These factors are reversed in TEL-AMLl negative cells to hinder EpoR expression.