Artykuły w czasopismach na temat „Erythropoietin”
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1
Rivera, Seth, Mihwa Pak, Miguel A. Lopez, Victoria Gabayan i Tomas Ganz. "Hepcidin Suppression Following Phlebotomy Is Regulated by an Erythropoietic Regulator Found in Serum." Blood 108, nr 11 (16.11.2006): 1554. http://dx.doi.org/10.1182/blood.v108.11.1554.1554.
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Abstract Increasing erythropoiesis requires a dramatic increase in iron absorption or the release of iron from tissue stores. Since the iron regulatory hormone hepcidin blocks both absorption and release from stores, it is suppressed during erythropoiesis. We have recently shown that hepcidin is primarily suppressed by an erythropoietic regulator rather then anemia, hypoxia, or erythropoietin (Pak et al, Blood, epub/in press). To further understand the regulation of hepcidin during erythropoiesis, we subjected groups of eight mice to phlebotomy and sacrificed them at various time points over 3 weeks. Hepcidin mRNA fell 25-fold by day 2 (p<0.001) and did not begin to rise until day 9. Hemoglobin rose well before hepcidin mRNA began to increase confirming that anemia was not the erythropoietic regulator. Serum iron never fell, excluding this as the erythropoietic regulator. Erythropoietin levels spiked early but returned to normal well before hepcidin. Reticulocyte counts increased shortly after the fall in hepcidin and remained elevated after hepcidin mRNA returned to normal. We therefore postulate that the erythropoietic iron regulator is either made by or in concert with early erythroid progenitor cells. Using primary hepatocytes treated with serum from erythropoietin stimulated or control mice, we also demonstrate that the erythropoietic regulator of hepcidin expression is present in the circulation. Experiments are underway to isolate the erythropoietic regulator of hepcidin from serum.
2
Zangari, Maurizio, Federica Cavallo, Keshava Prasad, Louis Fink, Sharon Coon, Bart Barlogie i Guido Tricot. "Erythropoietin Therapy and Venous Thromboembolic Events in Patients with Multiple Myeloma Receiving Chemotherapy with or without Thalidomide." Blood 108, nr 11 (16.11.2006): 3572. http://dx.doi.org/10.1182/blood.v108.11.3572.3572.
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Abstract Background: The association between the use of recombinant human erythropoietin (rHUEPO) and venous thromboembolic events (VTE) has been described in cancer patients treated with chemotherapy. A higher risk of VTE has also been observed with the concurrent use of erythropoiesis-stimulating agents and chemotherapy. Methods: We retrospectively analyzed VTE incidence and concurrent use of erythropoiesis-stimulating agents in patients with multiple myeloma (MM) enrolled in our Total Therapy 2 (TT2) study. TT2 included 4 monthly cycles of induction chemotherapy followed by tandem transplant. Patients were randomly assigned to receive Thalidomide or not during the whole treatment. Both arms otherwise received identical chemotherapy. Results: The charts of 599 of a total of 668 patients enrolled (90%) were reviewed; 284 patients received Thalidomide, 315 did not. With median age was 57 years, 59% were male, 24% had IgA myeloma. 62% of patients received erythropoietin (erythropoietin alpha 40000 U SQ/week) during the first 4 months of treatment. In thalidomide treated patients, VTE occurred in 33 out of 166 (20%) patients who concomitantly received administration of erythropoietic agents and in 38 out of 118 (32%) patients who did not receive erythropoietin (p=.025). Among patients not receiving thalidomide, VTE occurred in 18 out of 203 (8%) patients who received concomitant administration of erythropoietic agents and in 17 out of 112 (15%) patients who did not receive erythropoietin (p=.10). Conclusions: The development of thrombosis in patients enrolled on TTII protocol was not increased by the concomitant use of erythropoiesis-stimulating agents and thalidomide. Similarly, erythropoiesis-stimulating therapy did not affect VTE incidence in newly diagnosed myeloma patients treated with intensive chemotherapy without thalidomide.
3
Pak, Mihwa, Miguel A. Lopez, Victroia Gabayan, Tomas Ganz i Seth Rivera. "Suppression of hepcidin during anemia requires erythropoietic activity". Blood 108, nr 12 (1.12.2006): 3730–35. http://dx.doi.org/10.1182/blood-2006-06-028787.
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AbstractHepcidin, the principal iron regulatory hormone, regulates the absorption of iron from the diet and the mobilization of iron from stores. Previous studies indicated that hepcidin is suppressed during anemia, a response that would appropriately increase the absorption of iron and its release from stores. Indeed, in the mouse model, hepcidin-1 was suppressed after phlebotomy or erythropoietin administration but the suppression was reversed by inhibitors of erythropoiesis. The suppression of hepcidin necessary to match iron supply to erythropoietic demand thus requires increased erythropoiesis and is not directly mediated by anemia, tissue hypoxia, or erythropoietin.
4
Verhoef, Hans, Clive E. West, Rob Kraaijenhagen, Silas M. Nzyuko, Rose King, Mary M. Mbandi, Susanne van Laatum, Roos Hogervorst, Carla Schep i Frans J. Kok. "Malarial anemia leads to adequately increased erythropoiesis in asymptomatic Kenyan children". Blood 100, nr 10 (15.11.2002): 3489–94. http://dx.doi.org/10.1182/blood-2001-12-0228.
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Malarial anemia is associated with a shift in iron distribution from functional to storage compartments. This suggests a relative deficit in erythropoietin production or action similar to that observed in other infections. Our study in Kenyan children with asymptomatic malaria aimed at investigating whether malaria causes increased erythropoiesis, and whether the erythropoietic response appeared appropriate for the degree of resulting anemia. Longitudinal and baseline data were used from a trial with a 2 × 2 factorial design, in which 328 anemic Kenyan children were randomly assigned to receive either iron or placebo, and sulfadoxine-pyrimethamine or placebo. Erythropoiesis was evaluated by serum concentrations of erythropoietin and soluble transferrin receptor. Prospectively collected data showed that malarial infection resulted in decreased hemoglobin concentrations, and increased serum concentrations of erythropoietin and transferrin receptor. Conversely, disappearance of malarial antigenemia resulted in increased hemoglobin concentrations, and decreased concentrations of these serum indicators. Additionally, our baseline data showed that current or recent malarial infection is associated with increased serum concentrations of erythropoietin and transferrin receptor, and that these were as high as or perhaps even higher than values of children without malarial infection and without inflammation. Our findings indicate that in asymptomatic malaria, the erythropoietic response is adequate for the degree of anemia, and that inflammation probably plays no or only a minor role in the pathogenesis of the resulting anemia. Further research is needed to demonstrate the role of deficient erythropoietin production or action in the pathogenesis of the anemia of symptomatic malaria.
5
Dumitriu, Bogdan, Michael R. Patrick, Jane P. Petschek, Srujana Cherukuri, Ursula Klingmuller, Paul L. Fox i Véronique Lefebvre. "Sox6 cell-autonomously stimulates erythroid cell survival, proliferation, and terminal maturation and is thereby an important enhancer of definitive erythropoiesis during mouse development". Blood 108, nr 4 (15.08.2006): 1198–207. http://dx.doi.org/10.1182/blood-2006-02-004184.
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Abstract Erythropoiesis, the essential process of hematopoietic stem cell development into erythrocytes, is controlled by lineage-specific transcription factors that determine cell fate and differentiation and by the hormone erythropoietin that stimulates cell survival and proliferation. Here we identify the Sry-related high-mobility-group (HMG) box transcription factor Sox6 as an important enhancer of definitive erythropoiesis. Sox6 is highly expressed in proerythroblasts and erythroblasts in the fetal liver, neonatal spleen, and bone marrow. Mouse fetuses and pups lacking Sox6 develop erythroid cells slowly and feature misshapen, short-lived erythrocytes. They compensate for anemia by elevating the serum level of erythropoietin and progressively enlarging their erythropoietic tissues. Erythroid-specific inactivation of Sox6 causes the same phenotype, demonstrating cell-autonomous roles for Sox6 in erythroid cells. Sox6 potentiates the ability of erythropoietin signaling to promote proerythroblast survival and has an effect additive to that of erythropoietin in stimulating proerythroblast and erythroblast proliferation. Sox6 also critically facilitates erythroblast and reticulocyte maturation, including hemoglobinization, cell condensation, and enucleation, and ensures erythrocyte cytoskeleton long-term stability. It does not control adult globin and erythrocyte cytoskeleton genes but acts by stabilizing filamentous actin (F-actin) levels. Sox6 thus enhances erythroid cell development at multiple levels and thereby ensures adequate production and quality of red blood cells.
6
Yu, Xiaobing, Chyuan-Sheng Lin, Frank Costantini i Constance Tom Noguchi. "The human erythropoietin receptor gene rescues erythropoiesis and developmental defects in the erythropoietin receptor null mouse". Blood 98, nr 2 (15.07.2001): 475–77. http://dx.doi.org/10.1182/blood.v98.2.475.
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Erythropoietin and its receptor are required for definitive erythropoiesis and maturation of erythroid progenitor cells. Mice lacking the erythropoietin receptor exhibit severe anemia and die at about embryonic day 13.5. This phenotype can be rescued by the human erythropoietin receptor transgene. Animals expressing only the human erythropoietin receptor survived through adulthood with normal hematologic parameters and appeared to respond appropriately to induced anemic stress. In addition to restoration of erythropoiesis during development, the cardiac defect associated with embryos lacking the erythropoietin receptor was corrected and the increased apoptosis in fetal liver, heart, and brain in the erythropoietin receptor null phenotype was markedly reduced. These studies indicate that no species barrier exists between mouse and human erythropoietin receptor and that the human erythropoietin receptor transgene is able to provide specific expression in hematopoietic and other selected tissues to rescue erythropoiesis and other organ defects observed in the erythropoietin receptor null mouse.
7
Maekawa, Shun, i Takashi Kato. "Diverse of Erythropoiesis Responding to Hypoxia and Low Environmental Temperature in Vertebrates". BioMed Research International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/747052.
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Erythrocytes are responsible for transporting oxygen to tissue and are essential for the survival of almost all vertebrate animals. Circulating erythrocyte counts are tightly regulated and respond to erythrocyte mass and oxygen tension. Since the discovery of erythropoietin, the erythropoietic responses to environment and tissue oxygen tension have been investigated in mice and human. Moreover, it has recently become increasingly clear that various environmental stresses could induce the erythropoiesis via various modulating systems, while all vertebrates live in various environments and habitually adapt to environmental stress. Therefore, it is considered that investigations of erythropoiesis in vertebrates provide a lead to the various erythropoietic responses to environmental stress. This paper comparatively introduces the present understanding of erythropoiesis in vertebrates. Indeed, there is a wide range of variations in vertebrates’ erythropoiesis. This paper also focused on erythropoietic responses to environmental stress, hypoxia, and lowered temperature in vertebrates.
8
Baynes, RD, GK Reddy, YJ Shih, BS Skikne i JD Cook. "Serum form of the erythropoietin receptor identified by a sequence- specific peptide antibody [see comments]". Blood 82, nr 7 (1.10.1993): 2088–95. http://dx.doi.org/10.1182/blood.v82.7.2088.2088.
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Abstract The present investigation was undertaken to search for soluble forms of the erythropoietin receptor in human serum using polyclonal antibody against an amino terminal peptide sequence in the extracellular domain. This sequence was located adjacent to the amino terminus at residues 25- 38. When this antibody was used for Western blots of solubilized membranes from nucleated bone marrow cells, a protein consistent with native erythropoietin receptor was seen. Purified soluble ectodomain of the erythropoietin receptor displayed appropriate reactivity with this antibody. When sera from normal subjects and patients with a range of hematologic disorders were examined by Western blotting, a protein with a molecular mass of 34 Kd was detected in sera from patients with enhanced erythropoiesis including sickle cell anemia, thalassemia, and megaloblastic anemia. This protein was rarely detected in normal serum but appeared when normal subjects were treated with recombinant erythropoietin and disappeared after full treatment of patients with megaloblastic anemia due to vitamin B12 deficiency. The protein was not detected after myeloablation for bone marrow transplantation but appeared with marrow engraftment. Reactivity of this protein with the peptide antibody was competitively inhibited by the amino terminal peptide sequence. An additional 48 Kd protein was detected that showed minimal variation in intensity with differing degrees of erythropoietic activity. Detection of this protein could not be inhibited by the addition of synthetic peptide. Our findings indicate the presence of a soluble form of the erythropoietin receptor related to the extracellular domain that is highly correlated with enhanced erythropoiesis.
9
Baynes, RD, GK Reddy, YJ Shih, BS Skikne i JD Cook. "Serum form of the erythropoietin receptor identified by a sequence- specific peptide antibody [see comments]". Blood 82, nr 7 (1.10.1993): 2088–95. http://dx.doi.org/10.1182/blood.v82.7.2088.bloodjournal8272088.
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The present investigation was undertaken to search for soluble forms of the erythropoietin receptor in human serum using polyclonal antibody against an amino terminal peptide sequence in the extracellular domain. This sequence was located adjacent to the amino terminus at residues 25- 38. When this antibody was used for Western blots of solubilized membranes from nucleated bone marrow cells, a protein consistent with native erythropoietin receptor was seen. Purified soluble ectodomain of the erythropoietin receptor displayed appropriate reactivity with this antibody. When sera from normal subjects and patients with a range of hematologic disorders were examined by Western blotting, a protein with a molecular mass of 34 Kd was detected in sera from patients with enhanced erythropoiesis including sickle cell anemia, thalassemia, and megaloblastic anemia. This protein was rarely detected in normal serum but appeared when normal subjects were treated with recombinant erythropoietin and disappeared after full treatment of patients with megaloblastic anemia due to vitamin B12 deficiency. The protein was not detected after myeloablation for bone marrow transplantation but appeared with marrow engraftment. Reactivity of this protein with the peptide antibody was competitively inhibited by the amino terminal peptide sequence. An additional 48 Kd protein was detected that showed minimal variation in intensity with differing degrees of erythropoietic activity. Detection of this protein could not be inhibited by the addition of synthetic peptide. Our findings indicate the presence of a soluble form of the erythropoietin receptor related to the extracellular domain that is highly correlated with enhanced erythropoiesis.
10
Hankins, WD, J. Schooley i C. Eastment. "Erythropoietin, an autocrine regulator? Serum-free production of erythropoietin by cloned erythroid cell lines". Blood 68, nr 1 (1.07.1986): 263–68. http://dx.doi.org/10.1182/blood.v68.1.263.263.
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Abstract Production of lymphoid and myeloid growth regulatory factors by hematopoietic cells is well documented. On the other hand, the major site of production of erythropoietin (Epo), which regulates physiologic red blood cell development, is thought to be the kidney. Here we report the isolation of multiple erythroleukemia cell lines that produce erythropoietic factors and present extensive biological, immunologic, and biochemical evidence to document that the active agent is Epo. The erythropoietic activity was neutralized by Epo antiserum and exhibited physical properties indistinguishable from those of human and sheep Epo. Positive lines produced between 0.1 and 1.5 U/mL of Epo, which stimulated erythropoiesis in vivo and in vitro in nine biological assays. Twenty sublines derived from single cells were inducible for hemoglobin and spectrin synthesis. All the sublines produced Epo. Production of the hormone continued when the cells were seeded in the absence of serum. Our finding that multiple independent isolates produce Epo raises the possibility that Epo production by erythroid precursors may play a role in normal erythropoiesis or, alternatively, that Epo gene activation may be a relatively common occurrence that contributes to, or is associated with, certain forms of virus-induced leukemias.
11
Hankins, WD, J. Schooley i C. Eastment. "Erythropoietin, an autocrine regulator? Serum-free production of erythropoietin by cloned erythroid cell lines". Blood 68, nr 1 (1.07.1986): 263–68. http://dx.doi.org/10.1182/blood.v68.1.263.bloodjournal681263.
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Production of lymphoid and myeloid growth regulatory factors by hematopoietic cells is well documented. On the other hand, the major site of production of erythropoietin (Epo), which regulates physiologic red blood cell development, is thought to be the kidney. Here we report the isolation of multiple erythroleukemia cell lines that produce erythropoietic factors and present extensive biological, immunologic, and biochemical evidence to document that the active agent is Epo. The erythropoietic activity was neutralized by Epo antiserum and exhibited physical properties indistinguishable from those of human and sheep Epo. Positive lines produced between 0.1 and 1.5 U/mL of Epo, which stimulated erythropoiesis in vivo and in vitro in nine biological assays. Twenty sublines derived from single cells were inducible for hemoglobin and spectrin synthesis. All the sublines produced Epo. Production of the hormone continued when the cells were seeded in the absence of serum. Our finding that multiple independent isolates produce Epo raises the possibility that Epo production by erythroid precursors may play a role in normal erythropoiesis or, alternatively, that Epo gene activation may be a relatively common occurrence that contributes to, or is associated with, certain forms of virus-induced leukemias.
12
Fried, Walter. "Erythropoietin and erythropoiesis". Experimental Hematology 37, nr 9 (wrzesień 2009): 1007–15. http://dx.doi.org/10.1016/j.exphem.2009.05.010.
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Moritz, K. M., Gaik Bee Lim i E. M. Wintour. "Developmental regulation of erythropoietin and erythropoiesis". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, nr 6 (1.12.1997): R1829—R1844. http://dx.doi.org/10.1152/ajpregu.1997.273.6.r1829.
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It is well established that erythropoiesis occurs first in the yolk sac, then in the liver, subsequently moving to the bone marrow and, in rodents, the spleen during development. The origin of the erythropoietic precursors and some factors suggested to be important for the changing location of erythropoiesis are discussed in this review. Until recently, the major site of erythropoietin (Epo) production in the fetus was thought to be the liver, but studies have shown now that the Epo gene is expressed strongly in the fetal kidney, even in the temporary mesonephros. The metanephric Epo mRNA is upregulated by anemia, downregulated by glucocorticoids, and contributes substantially to circulating hormone levels in hemorrhaged ovine fetuses. Other sites of Epo and Epo receptor production, likely to have important actions during development, are the placenta and the brain.
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Obeagu, Emmanuel Ifeanyi, Getrude Uzoma Obeagu, Esther Ugo Alum i Okechukwu Paul-Chima Ugwu. "Understanding the Impact of HIV-Associated Bone Marrow Alterations on Erythropoiesis". INOSR Scientific Research 10, nr 1 (14.12.2023): 1–11. http://dx.doi.org/10.59298/inosrsr/2023/1.2.12222.
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Human Immunodeficiency Virus (HIV) infection presents a multifaceted challenge, extending beyond its primary impact on the immune system to affect various organ systems. Among these, the bone marrow, the primary site for hematopoiesis, undergoes substantial alterations during HIV infection, profoundly influencing erythropoiesis—the process of red blood cell production. Anemia, a prevalent hematologic complication in HIV-infected individuals, often serves as a marker of disease progression and impacts overall health outcomes. This paper aims to delve into the intricate relationship between HIV-associated bone marrow alterations and their consequential effects on erythropoiesis. The mechanisms underlying bone marrow changes in HIV infection, including direct viral effects, dysregulation of cytokine networks, and inflammatory processes, significantly disrupt the delicate balance necessary for efficient erythropoiesis. The impact of these alterations on erythropoiesis manifests through ineffective red blood cell production, decreased erythropoietin responsiveness, and shortened red blood cell lifespan. Chronic inflammation further complicates erythropoietic processes, contributing to the development and perpetuation of anemia in HIV-infected individuals. Therapeutic interventions encompass a multifaceted approach, including antiretroviral therapy (ART) to control viral replication, erythropoiesis-stimulating agents, and adjunctive nutritional support to manage anemia. However, emerging research targeting bone marrow microenvironmental factors and novel agents stimulating erythropoiesis offer promising avenues for future therapeutic development. Keywords: HIV, bone marrow, erythropoiesis, erythropoietin, antiretroviral therapy
15
Piperno, Alberto, Stefania Galimberti, Raffaella Mariani, Sara Pelucchi, Giulia Ravasi, Carolina Lombardi, Grzegorz Bilo i in. "Modulation of hepcidin production during hypoxia-induced erythropoiesis in humans in vivo: data from the HIGHCARE project". Blood 117, nr 10 (10.03.2011): 2953–59. http://dx.doi.org/10.1182/blood-2010-08-299859.
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AbstractIron is tightly connected to oxygen homeostasis and erythropoiesis. Our aim was to better understand how hypoxia regulates iron acquisition for erythropoiesis in humans, a topic relevant to common hypoxia-related disorders. Forty-seven healthy volunteers participated in the HIGHCARE project. Blood samples were collected at sea level and after acute and chronic exposure to high altitude (3400-5400 m above sea level). We investigated the modifications in hematocrit, serum iron indices, erythropoietin, markers of erythropoietic activity, interleukin-6, and serum hepcidin. Hepcidin decreased within 40 hours after acute hypoxia exposure (P < .05) at 3400 m, reaching the lowest level at 5400 m (80% reduction). Erythropoietin significantly increased (P < .001) within 16 hours after hypoxia exposure followed by a marked erythropoietic response supported by the increased iron supply. Growth differentiation factor-15 progressively increased during the study period. Serum ferritin showed a very rapid decrease, suggesting the existence of hypoxia-dependent mechanism(s) regulating storage iron mobilization. The strong correlation between serum ferritin and hepcidin at each point during the study indicates that iron itself or the kinetics of iron use in response to hypoxia may signal hepcidin down-regulation. The combined and significant changes in other variables probably contribute to the suppression of hepcidin in this setting.
16
Coussons, P. J., S. Baig, C. Fanutti i R. Grant. "Novel tissue remodelling roles for human recombinant erythropoietin". Biochemical Society Transactions 33, nr 5 (26.10.2005): 1129–30. http://dx.doi.org/10.1042/bst0331129.
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rHuEPO (recombinant human erythropoietin) is a haemopoietic growth factor and a primary regulator of erythropoiesis that is used for the treatment of chronic anaemia associated with RA (rheumatoid arthritis). Erythropoietin also appears to modulate a broad array of cellular processes, including progenitor stem-cell development, cellular integrity, angiogenesis and oxidative damage. These diverse activities suggest the exciting possibility of multiple roles for rHuEPO therapy in a variety of disorders other than RA, including cerebral ischaemia, myocardial infarction, chronic congestive heart failure and cancer. Thus it appears that rHuEPO may be a pleiotropic agent, capable of influencing tissue remodelling independently of its established erythropoietic role. Whereas these effects may be largely beneficial, dose-related side effects could have implications for the safe therapeutic use of rHuEPO and its illegal use as a performance-enhancing agent in endurance sports.
17
Goodnough, Lawrence T., Barry Skikne i Carlo Brugnara. "Erythropoietin, iron, and erythropoiesis". Blood 96, nr 3 (1.08.2000): 823–33. http://dx.doi.org/10.1182/blood.v96.3.823.
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Abstract Recent knowledge gained regarding the relationship between erythropoietin, iron, and erythropoiesis in patients with blood loss anemia, with or without recombinant human erythropoietin therapy, has implications for patient management. Under conditions of significant blood loss, erythropoietin therapy, or both, iron-restricted erythropoiesis is evident, even in the presence of storage iron and iron oral supplementation. Intravenous iron therapy in renal dialysis patients undergoing erythropoietin therapy can produce hematologic responses with serum ferritin levels up to 400 μg/L, indicating that traditional biochemical markers of storage iron in patients with anemia caused by chronic disease are unhelpful in the assessment of iron status. Newer measurements of erythrocyte and reticulocyte indices using automated counters show promise in the evaluation of iron-restricted erythropoiesis. Assays for serum erythropoietin and the transferrin receptor are valuable tools for clinical research, but their roles in routine clinical practice remain undefined. The availability of safer intravenous iron preparations allows for carefully controlled studies of their value in patients undergoing erythropoietin therapy or experiencing blood loss, or both.
18
Goodnough, Lawrence T., Barry Skikne i Carlo Brugnara. "Erythropoietin, iron, and erythropoiesis". Blood 96, nr 3 (1.08.2000): 823–33. http://dx.doi.org/10.1182/blood.v96.3.823.015k49_823_833.
Pełny tekst źródłaStreszczenie:
Recent knowledge gained regarding the relationship between erythropoietin, iron, and erythropoiesis in patients with blood loss anemia, with or without recombinant human erythropoietin therapy, has implications for patient management. Under conditions of significant blood loss, erythropoietin therapy, or both, iron-restricted erythropoiesis is evident, even in the presence of storage iron and iron oral supplementation. Intravenous iron therapy in renal dialysis patients undergoing erythropoietin therapy can produce hematologic responses with serum ferritin levels up to 400 μg/L, indicating that traditional biochemical markers of storage iron in patients with anemia caused by chronic disease are unhelpful in the assessment of iron status. Newer measurements of erythrocyte and reticulocyte indices using automated counters show promise in the evaluation of iron-restricted erythropoiesis. Assays for serum erythropoietin and the transferrin receptor are valuable tools for clinical research, but their roles in routine clinical practice remain undefined. The availability of safer intravenous iron preparations allows for carefully controlled studies of their value in patients undergoing erythropoietin therapy or experiencing blood loss, or both.
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Diwan, Abhinav, Andrew G. Koesters, Amy M. Odley, Theodosia A. Kalfa i Gerald W. Dorn. "Enhanced Erythroblast Mobilization in Nix-Deficient Mice Confers Resistance to Phenylhydrazine-Induced Anemia Despite Accelerated Erythrocyte Turnover." Blood 110, nr 11 (16.11.2007): 3659. http://dx.doi.org/10.1182/blood.v110.11.3659.3659.
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Abstract Steady-state and dynamic regulation of erythrocyte production occurs by altering the balance of cell-survival versus apoptosis signaling in maturing erythroblasts. Previously, the pro-apoptotic factor Nix was identified as a critical death signal in normal erythropoietic homeostasis, acting in opposition to erythroblast-survival signaling by erythropoietin and Bcl-xl. However, the role of Nix in stress-erythropoiesis is not known. Here, by comparing the consequences of erythropoietin administration, acute phenylhydrazine-induced anemia, and aging in wild-type and Nix-deficient mice, we show that complete absence of Nix, or its genetic ablation specifically in hematopoietic cells, mimics the effects of erythropoietin (Epo). Both Nix ablation and Epo treatment increase early erythroblasts in spleen and bone marrow and increase the number of circulating reticulocytes, while maintaining a pool of mature erythroblasts as an “erythropoietic reserve”. As compared with WT, Nix null mice develop polycythemia more rapidly after Epo treatment, consistent with enhanced sensitivity to erythropoietin observed in vitro. After phenylhydrazine administration, anemia in Nix-deficient mice is less severe and recovers more rapidly than in WT mice, despite lower endogenous Epo levels. Anemic stress depletes mature erythroblasts in both WT and Nix null mice, but Nix null mice with basal erythroblastosis are resistant to anemic stress. These findings show that Nix null mice have greatly expanded erythroblast reserve and respond normally to Epo- and anemia-stimulated induction of erythropoiesis. However, the hematocrits of young adult Nix null mice are not elevated, and these mice paradoxically develop anemia as they age with decreased hemoglobin content (10g/dl) and hematocrit (36%; at 80±3 weeks of age) compared to WT mice (13g/dl and 46%; 82±5 weeks of age), inspite of persistent erythoblastosis observed in the bone marrow and spleen. Nix null erythrocytes, which are macrocytic and exhibit membrane abnormalities typically seen in immature cells or with accelerated erythropoiesis, demonstrate shorter life span with a half life of 5.2±0.6 days in the peripheral circulation by in vivo biotin labeling (as compared with a half life of 11.7±0.9 days in WT), and increased osmotic fragility as compared with normal erythrocytes. This suggests that production and release of large numbers of reticulocytes in Nix null mice can decrease erythrocyte survival. To rule out a non-hematopoietic consequence of Nix ablation that contributes to or causes increased erythrocyte fragility and in vivo consumption, such as primary hypersplenism, we undertook Tie2-Cre mediated conditional Nix gene ablation. Nixfl/fl + Tie2-Cre mice (hematopoietic-cell specific Nix null) develop erythroblastosis with splenomegaly, reticulocytosis, absence of polycythemia and increased erythrocyte fragility; suggesting that erythroblastosis and accelerated erythrocyte turnover are a primary consequence of Nix ablation in hematopoietic cells. Hence, dis-inhibition of erythropoietin-mediated erythroblast survival pathways by Nix ablation enhances steady-state and stress-mediated erythropoiesis.
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Chateauvieux, S., C. Grigorakaki, F. Morceau, M. Dicato i M. Diederich. "Erythropoietin, erythropoiesis and beyond". Biochemical Pharmacology 82, nr 10 (listopad 2011): 1291–303. http://dx.doi.org/10.1016/j.bcp.2011.06.045.
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Okaji, Yurai, Chiemi Nishida, Ismael Gritli, Yoshihiko Tashiro, Makiko Ohki, Koichi Hattori i Beate Heissig. "Plasminogen Deficiency Impairs Erythropoietic Recovery Capacity In Male C57BL/6J Mice through Testosterone Defect". Blood 116, nr 21 (19.11.2010): 3212. http://dx.doi.org/10.1182/blood.v116.21.3212.3212.
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Abstract Abstract 3212 Plasminogen (Plg), a classical fibrinolytic factor, is essential for maintaining homeostasis of blood coagulation, and has important roles in wound healing as well as pathophysiology of atherosclerosis, cancer and Alzheimer's disease. Recently, we have shown that the activation of the Plg fibrinolytic pathway is critical for hematopoietic regeneration from stem cells after myelosuppression. Here, we investigated the role of Plg in regulating erythropoiesis. Male and female C57BL/6J mice with normal or homozygously disrupted Plg genes were used under steady state conditions and in a model of acute erythropoietic stress selectively induced by intravenous injection of the hemolytic drug phenylhydrazine hydrochloride. Orbital vein blood, bone marrow and spleen were obtained to determine erythropoietic parameters. In addition, testosterone concentrations were measured in murine serum. Normochromic normocytic anemia was found in Plg-/- mice under steady state conditions. Microscopic evaluation of blood smears revealed the presence of altered erythrocytes, such as acanthocytes, echinocytes (burr cells) and to lesser extent schistocytes. In addition, flow cytometry of intravenously injected autologous erythrocytes, labeled with a fluorescent probe, showed significantly shortened erythrocyte lifespan, suggestive of hemolysis as a cause of the anemia. In concordance, there was an increase in plasma erythropoietin with augmented reticulocyte counts, erythroid burst forming units in bone marrow, and finally erythroid progenitors in spleens, which were significantly enlarged, suggestive of extramedullar erythropoiesis. Interestingly, the intensity of compensatory erythropoiesis was higher in Plg-/- female mice, resulting in lesser hematocrit decrease when compared to that observed in Plg-/- male mice. In addition, similar gender differences could be observed in a model of acute erythropoietic stress. Concretely, acute hemolytic anemia induced by intravenous injection of phenylhydrazine hydrochloride resulted in a significant erythrocyte recovery delay in Plg-/- male mice that, in contrast, was not as profound in Plg-/- female mice. To understand the reason for the observed gender differences, a competitive enzyme immunoassay was employed to measure serum concentrations of testosterone. As a result, a significant decrease in serum testosterone levels was detected in Plg-/- male mice. In summary, we found that Plg plays important role in maintaining normal lifespan of erythrocytes by preventing their mechanical alteration by microangiopathy from abnormal fibrin deposition. In addition, given that testosterone is well known to regulate erythropoiesis, through increasing erythropoietin levels as well as having non-erythropoietin stimulating effects, our present results suggest that Plg might also play roles in regulating erythropoiesis through being important for normal testosterone production. Disclosures: No relevant conflicts of interest to declare.
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Correnti, Margherita, Elena Gammella, Gaetano Cairo i Stefania Recalcati. "Iron Mining for Erythropoiesis". International Journal of Molecular Sciences 23, nr 10 (10.05.2022): 5341. http://dx.doi.org/10.3390/ijms23105341.
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Iron is necessary for essential processes in every cell of the body, but the erythropoietic compartment is a privileged iron consumer. In fact, as a necessary component of hemoglobin and myoglobin, iron assures oxygen distribution; therefore, a considerable amount of iron is required daily for hemoglobin synthesis and erythroid cell proliferation. Therefore, a tight link exists between iron metabolism and erythropoiesis. The liver-derived hormone hepcidin, which controls iron homeostasis via its interaction with the iron exporter ferroportin, coordinates erythropoietic activity and iron homeostasis. When erythropoiesis is enhanced, iron availability to the erythron is mainly ensured by inhibiting hepcidin expression, thereby increasing ferroportin-mediated iron export from both duodenal absorptive cells and reticuloendothelial cells that process old and/or damaged red blood cells. Erythroferrone, a factor produced and secreted by erythroid precursors in response to erythropoietin, has been identified and characterized as a suppressor of hepcidin synthesis to allow iron mobilization and facilitate erythropoiesis.
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Noguchi, Constance Tom, Heather Marie Rogers, Li Wang i Ruifeng Teng. "Erythropoietin Increases Erythropoiesis, Metabolism and Weight Loss In Mice". Blood 122, nr 21 (15.11.2013): 946. http://dx.doi.org/10.1182/blood.v122.21.946.946.
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Abstract Erythropoietin is required for erythroid progenitor cell survival, proliferation and differentiation. Increasing evidence suggests that erythropoietin treatment in mice can stimulate erythropoiesis and also affect metabolic processes in a dose dependent manner. For example, medium to high dose erythropoietin treatment (600 U/kg or 3000 U/kg) in leptin deficient obese (ob/ob) mice three times a week for three weeks or more results in the expected increase in hematocrit as well as decrease in accumulated body fat and improved glucose tolerance. Phlebotomy to maintain normal hematocrit demonstrated that erythropoietin regulation of body weight was not dependent on increased red cell mass. In non-obese wild type C57BL/6 mice, erythropoietin treatment also demonstrated the expected increase in hematocrit as well as a 15% reduction in body weight and decreased fasting blood glucose. Erythropoietin receptor is expressed at the highest level in erythroid progenitor cells. The link between increased metabolism and erythropoietin stimulated erythroid differentiation was suggested by the increased oxygen consumption rate observed in vitro in primary cultures of erythropoietin stimulated erythroid progenitor cells. Erythropoietin also stimulated glucose uptake in differentiating erythroid progenitor cells in a dose dependent manner. Glucose uptake decreased with the down regulation of erythropoietin receptor during terminal differentiation. Relatively high erythropoietin receptor expression and erythropoietin activity that may also contribute to erythropoietin metabolic activity has been observed in non-hematopoietic mouse tissue including the hypothalamus and white adipose tissue (Teng R, Gavrilova O et al., Nat Commun 2011). The hypothalamus contributes importantly to appetite regulation and mice treated with erythropoietin exhibited a decrease in food intake compared with saline control. We found that pair-feeding decreased body weight and fat mass, and improved glucose tolerance, but no more than half that observed with erythropoietin treatment, providing evidence that erythropoietin regulation of food intake accounts for only part of the metabolic response observed with erythropoietin treatment. Adipocytes isolated from white adipose tissue in erythropoietin treated mice showed an increase in oxygen consumption compared with vehicle treated or pair-fed mice. To assess the role of direct erythropoietin response of white adipose tissue in regulation of fat mass accumulation, we engineered mice with targeted deletion of erythropoietin receptor in adipose tissue. Erythropoietin treatment gave rise to the expected increase in hematocrit but resulted in a reduced decrease in body weight compared with saline treatment. These data show that erythropoietin treatment can stimulate cell oxygen consumption and can contribute to regulation of metabolism and body weight in mice. Erythropoietin receptor expression on erythroid progenitor cells provides for erythropoietin response to promote erythropoiesis and increase cell metabolic activity including glucose uptake and oxygen consumption. In non-hematopoietic tissue, erythropoietin receptor expression further contributes to erythropoietin regulated metabolic activity such as control of food intake attributed in part to hypothalamus response and modulation of fat mass affected by direct erythropoietin response in white adipose tissue. Therefore, in addition to its critical role in promoting erythropoiesis, erythropoietin can contribute to metabolic homeostasis via its activity in erythroid tissue and beyond. Disclosures: No relevant conflicts of interest to declare.
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Georgieff, M. K., R. L. Schmidt, M. M. Mills, W. J. Radmer i J. A. Widness. "Fetal iron and cytochrome c status after intrauterine hypoxemia and erythropoietin administration". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 262, nr 3 (1.03.1992): R485—R491. http://dx.doi.org/10.1152/ajpregu.1992.262.3.r485.
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Chronic fetal hypoxemia stimulates erythropoiesis and may result in a redistribution of fetal iron from plasma into erythrocytes. We studied the response of fetal plasma erythropoietin (Ep) to hypoxemia, the role of Ep in stimulating erythropoiesis in utero, and the effect of augmented erythropoiesis on fetal plasma Ep and iron and tissue cytochrome c concentrations in 19 chronically instrumented late-gestation fetal sheep. The fetuses were stimulated to produce 28 erythropoietic responses after exposure to 1) acute hypoxemia (1-5 days), 2) chronic hypoxemia (greater than 7 days), and/or 3) administration of 1,500 U recombinant human Ep concurrently during normoxemia. Plasma Ep peaked less than 12 h after the onset of hypoxemia or Ep bolus. Plasma iron decreased 24-48 h later and returned to baseline 48-96 h after normalization of Ep levels to baseline. The plasma iron response was directly related to the erythropoietin stimulus (r = 0.79, P less than 0.001) and inversely related to liver iron concentration at death (r = -0.84, P less than 0.001). Nine fetuses with depleted liver iron concentrations at autopsy had significantly lower heart and skeletal muscle iron concentrations compared with animals with 10% of control liver iron remaining. Skeletal muscle and heart iron and cytochrome c concentrations were significantly correlated. Ep has a potent biological effect on fetal erythropoiesis and iron metabolism. Augmented fetal erythropoiesis, mediated by Ep, results in decreased plasma iron, hepatic storage iron, and skeletal and cardiac muscle iron and cytochrome c. The model potentially explains the iron abnormalities found in newborn infants after fetal hypoxia.
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McGrowder, Donovan, Paul Brown, Ruby Lisa Alexander-Lindo, Shirley Budall, Rachael Irving i Lorenzo Gordon. "The Use of Soluble Transferrin Receptor in the Detection of rHuEPO abuse in Sports". Biochemistry Insights 3 (styczeń 2010): BCI.S3943. http://dx.doi.org/10.4137/bci.s3943.
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Erythropoietin (EPO) increases the number of circulating erythrocytes and muscle oxygenation. The recombinant forms of EPO have indiscriminately been used by athletes, mainly in endurance sports to increase their erythrocytes concentration, thus generating a better delivery of oxygen to the muscle tissue. The administration of recombinant human erythropoietin (rHuEPO) except for therapeutic use was prohibited by the International Olympic Committee (IOC) and its unauthorized use considered as doping. In the last few years, a number of studies using parameters indicative of accelerated erythropoiesis have investigated a number of indirect methods for the detection of rHuEPO abuse. No single indirect marker has been found that can satisfactorily demonstrated rHuEPO misuse. Soluble transferrin receptor (sTfR) is a new marker of iron status and erythropoietic activity. It has been included in multivariable blood testing models for the detection of performance enhancing EPO abuse in sports. Indirect markers of altered erythropoiesis give reliable evidence of current or discontinued rHuEPO usage. This review describes the physical, biological and pharmacokinetic properties of endogenous EPO and its recombinant form. It also discusses the available strategies for the detection of rHuEPO abuse in sports, involving the use of sTfR concentration directly or in mathematical multivariate models.
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Giordano, Giulio, Patrizia Mondello, Rosa Tambaro, Nicola Perrotta, Fabio D'amico, Giuseppe Berardi, Bruno Carabellese i Francesco Equitani. "Originator Erythropoietin Alpha Vs Biosimilar Erythropoietin Alpha vs Erythropoietin Zed Plus Liposomial Iron and b12 and Folates in Patients with Refractory Anemia. Five Center Retrospective Study". Blood 124, nr 21 (6.12.2014): 4872. http://dx.doi.org/10.1182/blood.v124.21.4872.4872.
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Abstract Background Biosimilar drugs, including erythropoirtin zed, have a similar, but usually not inferior although not hidentical effects of originator drugs. Safety is hidentical to originator drugs. Aims Aim of this study is to verify if in MDS patient with refractory anemia biosimilar erythropoietin alpha and erythropoietin zed, are not inferior to erythropoietin alpha in terms of safety, efficacy and costs. Methods This study is a retrospective study.Between july 2008 and december 2013, 101 patients affected by refractory anemia were studied.Median follow-up was 16 months (R10-28). Patients received in group A erythropoietin alpha 40000 IU sc/weekly. In group B patient received biosimilar erythropoietin alpha 40000 IU sc/weekly. In group C patient received biosimilar erythropoietin zed 40000 IU sc/weekly. In all three arms patients received liposomial iron (Sideral®) 14 mg 2 tablets orally/day calcium levofolinate 7.5 mg/day orally + Vitamin B12: 400 mg/day orally. In group A median age was 70 years (R63-73), M/F: 15/28. In group B median age was 64 years (R60-70), M/F: 24/19. In group C median age was 68 years (R62-73), M/F: 10/5.IPSS was low in 30 patients and int-1 in 12 patients, karyotype showed –Y in two patient, del 20q in one patient, trisomy 8 in two patients in group A. IPSS was low in 32 patients and int-1 in 10 patients, karyotype showed –Y in one patients, del 20q in one patient in group B.IPSS was low in 11 patients and int-1 in 4 patients, karyotype was normal in 9 patients and not evaluable in 6 patients. Patients with 5q- were excluded from this study. Median level of haemoglobin was 9 g/dl in group A (R8-11), 8.7 g/dl (R8.5-10.5) in group B and 8.5 in group C. Cost of every month of erythropoietinic therapy was calculed dividing for each patient the sum of complete erythropoietic therapy for each month of follow-up, then in each group of patients median cost of erythropoietic therapy was calculed. Results Group A patients increased Hb level of 1 g/dl after a median time of 5 weeks (R4-9), after a median time of 3.5 weeks (R3-8) in group B and after a memedian time of 4 weeks in group C. No relevant side effects were observed in all three groups groups. Erythropoietin alpha was reduced in group A because Hb achieved a level > 12g/dl after a median of 12 weeks (R 4-18).Biosimilar erythropoietin alpha was reduced in group B because Hb achieved a level > 12g/dl after a median of 10 weeks (R 3-16). Erythropoietin zed was reduced in group C because Hb achieved a level > 12g/dl after a median of 9.5 weeks (R 3-15). In group A maintenance dose was administered with a median of every two weeks (2-4), in group B maintenance dose was administered with a median of every three weeks (2-5), in group C maintenance dose was administered with a median of every three weeks (2-4). Median cost for every month of erythropoietic therapy was 1536 euros/month (R1240-1850) in group A, 1354 euros/month (R954-1550) in group B, 1300 euros/month (R1300-1380) in group C. Five patients need transfusion support in group A,6 patients need transfusion support in group B and 5 in group C. Summary/Conclusion Biosimilar erythropoietin alpha and erythropoietin zed plus liposomial iron (Sideral®) and B12 and folates support seems to be safe, feasible, probably equally cost-effective and substantially not inferior to classical erythropoietin alpha support in patients affected by refractory anemia. This study needs confifrmation on a larger cohort of patients. Disclosures No relevant conflicts of interest to declare.
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Coviello, Andrea D., Beth Kaplan, Kishore M. Lakshman, Tai Chen, Atam B. Singh i Shalender Bhasin. "Effects of Graded Doses of Testosterone on Erythropoiesis in Healthy Young and Older Men". Journal of Clinical Endocrinology & Metabolism 93, nr 3 (1.03.2008): 914–19. http://dx.doi.org/10.1210/jc.2007-1692.
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Abstract Context: Erythrocytosis is a dose-limiting adverse effect of testosterone therapy, especially in older men. Objective: Our objective was to compare the dose-related changes in hemoglobin and hematocrit in young and older men and determine whether age-related differences in erythropoietic response to testosterone can be explained by changes in erythropoietin and soluble transferrin receptor (sTfR) levels. Design: We conducted a secondary analysis of data from a testosterone dose-response study in young and older men who received long-acting GnRH agonist monthly plus one of five weekly doses of testosterone enanthate (25, 50, 125, 300, or 600 mg im) for 20 wk. Setting: The study took place at a General Clinical Research Center. Participants: Participants included 60 older men aged 60–75 yr and 61 young men aged 19–35 yr. Outcome Measures: Outcome measures included hematocrit and hemoglobin and serum erythropoietin and sTfR levels. Results: Hemoglobin and hematocrit increased significantly in a linear, dose-dependent fashion in both young and older men in response to graded doses of testosterone (P < 0.0001). The increases in hemoglobin and hematocrit were significantly greater in older than young men. There was no significant difference in percent change from baseline in erythropoietin or sTfR levels across groups in either young or older men. Changes in erythropoietin or sTfR levels were not significantly correlated with changes in total or free testosterone levels. Conclusions: Testosterone has a dose-dependent stimulatory effect on erythropoiesis in men that is more pronounced in older men. The testosterone-induced rise in hemoglobin and hematocrit and age-related differences in response to testosterone therapy may be mediated by factors other than erythropoietin and sTfR.
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Piron, Maude, Martine Loo, André Gothot, Françoise Tassin, Georges Fillet i Yves Beguin. "Cessation of intensive treatment with recombinant human erythropoietin is followed by secondary anemia". Blood 97, nr 2 (15.01.2001): 442–48. http://dx.doi.org/10.1182/blood.v97.2.442.
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Abstract Little information is available on the evolution of erythropoiesis after interruption of recombinant human erythropoietin (rHuEpo) therapy. Iron-overloaded rats received 20 daily injections of rHuEpo. During treatment, reticulocytes, soluble transferrin receptor (sTfR), and hematocrit increased progressively. This was accompanied by a substantial expansion of spleen erythropoiesis but a decrease in the bone marrow. Five weeks after treatment, rats developed a significant degree of aregenerative anemia. Erythropoietic activity, as assessed by reticulocytes, sTfR, erythroid cellularity, iron incorporation into heme, and the number of erythroid colonies, was severely depressed 3 weeks after cessation of rHuEpo. This was followed by regeneration of erythroblasts and reticulocytes at weeks 6 to 7 post-Epo, but erythroid progenitors recovered only partially by that time. The anemia was definitely corrected 2 months after cessation of rHuEpo treatment. Serum Epo levels remained elevated for several weeks, but the sensitivity of marrow erythroid precursors to Epo was preserved. No rat antibodies to rHuEpo were detected, and serum from post-Epo animals did not exert any inhibitory activity on erythropoiesis. In conclusion, after cessation of intensive rHuEpo therapy, there was a strong inhibition of erythropoietic activity with secondary anemia followed by late recovery. This was not due to antibodies or other soluble inhibitory factors, a defect in endogenous Epo production, or a loss of sensitivity to Epo. This may rather represent intrinsic erythroid marrow exhaustion, mostly at the level of erythroid progenitors but also at later stages of erythropoiesis.
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Ghezzi, Pietro, Myriam Bernaudin, Roberto Bianchi i Klas Blomgren. "Erythropoietin: not just about erythropoiesis". Lancet 375, nr 9732 (czerwiec 2010): 2142. http://dx.doi.org/10.1016/s0140-6736(10)60992-0.
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Goodnough, Lawrence Tim. "Erythropoietin and iron-restricted erythropoiesis". Experimental Hematology 35, nr 4 (kwiecień 2007): 167–72. http://dx.doi.org/10.1016/j.exphem.2007.01.026.
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KENDALL, R. G., I. CAVILL i D. R. NORFOLK. "Erythropoietin Consumption during Stimulated Erythropoiesis". Annals of the New York Academy of Sciences 718, nr 1 (26.02.2008): 350–52. http://dx.doi.org/10.1111/j.1749-6632.1994.tb55737.x.
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Debeljak, Nataša, i Arthur J. Sytkowski. "Erythropoietin and erythropoiesis stimulating agents". Drug Testing and Analysis 4, nr 11 (16.04.2012): 805–12. http://dx.doi.org/10.1002/dta.1341.
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Bullock, Grant C., Lorrie L. Delehanty, Anne-Laure Talbot, Sara L. Gonias, Wing-Hang Tong, Tracey A. Rouault, Brian Dewar, Jeffrey M. Macdonald, Jason J. Chruma i Adam N. Goldfarb. "Iron control of erythroid development by a novel aconitase-associated regulatory pathway". Blood 116, nr 1 (8.07.2010): 97–108. http://dx.doi.org/10.1182/blood-2009-10-251496.
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AbstractHuman red cell differentiation requires the action of erythropoietin on committed progenitor cells. In iron deficiency, committed erythroid progenitors lose responsiveness to erythropoietin, resulting in hypoplastic anemia. To address the basis for iron regulation of erythropoiesis, we established primary hematopoietic cultures with transferrin saturation levels that restricted erythropoiesis but permitted granulopoiesis and megakaryopoiesis. Experiments in this system identified as a critical regulatory element the aconitases, multifunctional iron-sulfur cluster proteins that metabolize citrate to isocitrate. Iron restriction suppressed mitochondrial and cytosolic aconitase activity in erythroid but not granulocytic or megakaryocytic progenitors. An active site aconitase inhibitor, fluorocitrate, blocked erythroid differentiation in a manner similar to iron deprivation. Exogenous isocitrate abrogated the erythroid iron restriction response in vitro and reversed anemia progression in iron-deprived mice. The mechanism for aconitase regulation of erythropoiesis most probably involves both production of metabolic intermediates and modulation of erythropoietin signaling. One relevant signaling pathway appeared to involve protein kinase Cα/β, or possibly protein kinase Cδ, whose activities were regulated by iron, isocitrate, and erythropoietin.
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Wu, H., S. H. Lee, J. Gao, X. Liu i M. L. Iruela-Arispe. "Inactivation of erythropoietin leads to defects in cardiac morphogenesis". Development 126, nr 16 (15.08.1999): 3597–605. http://dx.doi.org/10.1242/dev.126.16.3597.
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Erythropoietin is an essential growth factor that promotes survival, proliferation, and differentiation of mammalian erythroid progenitor cells. Erythropoietin(−/−) and erythropoietin receptor(−/−) mouse embryos die around embryonic day 13.5 due, in part, to failure of erythropoiesis in the fetal liver. In this study, we demonstrated a novel role of erythropoietin and erythropoietin receptor in cardiac development in vivo. We found that erythropoietin receptor is expressed in the developing murine heart in a temporal and cell type-specific manner: it is initially detected by embryonic day 10.5 and persists until day 14.5. Both erythropoietin(−/−) and erythropoietin receptor(−/−) embryos suffered from ventricular hypoplasia at day 12–13 of gestation. This defect appears to be independent from the general state of hypoxia and is likely due to a reduction in the number of proliferating cardiac myocytes in the ventricular myocardium. Cell proliferation assays revealed that erythropoietin acts as a mitogen in cells isolated from erythropoietin(−/−) mice, while it has no effect in hearts from erythropoietin receptor(−/−) animals. Erythropoietin(−/−) and erythropoietin receptor(−/−) embryos also suffered from epicardium detachment and abnormalities in the vascular network. Finally, through a series of chimeric analysis, we provided evidence that erythropoietin acts in a manner which is non-cell-autonomous. Our results elucidate a novel role of erythropoietin in cardiac morphogenesis and suggest a combination of anemia and cardiac failure as the cause of embryonic lethality in the erythropoietin(−/−) and erythropoietin receptor(−/−) animals.
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Myllymäki, Mikko, Jenni Määttä, Elitsa Dimova, Valerio Izzi, Timo Väisänen, Johanna Myllyharju, Peppi Koivunen i Raisa Serpi. "Extramedullary Erythropoiesis in Spleen of HIF Prolyl 4-Hydroxylase-2 Deficient Mice Is Mediated By Notch Signaling Downregulation". Blood 128, nr 22 (2.12.2016): 2656. http://dx.doi.org/10.1182/blood.v128.22.2656.2656.
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Abstract Erythrocytosis, an increase in absolute red cell mass, is mainly driven by erythropoietin, while hypoxia-inducible factor (HIF) regulates the expression of a number of genes involved in it, including erythropoietin. Mutations in HIF prolyl 4-hydroxylase 2 (HIF-P4H-2/PHD2/EGLN1), the major regulator of the stability of HIFα subunits, are found in familiar erythrocytosis, and large-spectrum conditional inactivation of HIF-P4H-2 in mice leads to severe erythrocytosis and premature death. Although bone marrow is the primary site for erythropoiesis, spleen retains a capability for extramedullary erythropoiesis. We studied HIF-P4H-2 hypomorphic mice (Hif-p4h-2gt/gt) which show slightly induced erythropoiesis only upon aging despite no increased erythropoietin levels. Spleen was identified as the site of extramedullary erythropoiesis in these mice. Hematopoietic stem cells (HSCs) from spleens of the Hif-p4h-2gt/gt mice showed increased growth of BFU-Es and the mice were protected against anemia by induced extramedullary erythropoiesis. HIF-1α and HIF-2α were stabilized in the spleens, while the Notch ligands and target Jag1, Jag2, Dll1 and Hes1 became downregulated upon aging dependent on HIF-2α. Inhibition of Notch signaling in wild-type spleen HSCs phenocopied the increased growth of BFU-Es in the Hif-p4h-2gt/gt mice. We conclude that HIFα stabilization can mediate non-erythropoietin-driven extramedullary erythropoiesis in the spleen via altered Notch signaling. Disclosures Myllyharju: FibroGen Inc.: Equity Ownership, Research Funding.
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Leonteva, E. V., i N. D. Savenkova. "Research of the level of erythropoietin and hypoxia-inducible factor 1-alpha in the blood of children and adolescents with anemia at stage C1–5 of chronic kidney disease". Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 65, nr 1 (6.03.2020): 77–85. http://dx.doi.org/10.21508/1027-4065-2020-65-1-77-85.
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Purpose. To examine the indicators of iron deficiency, the levels of hemoglobin, erythropoietin, hypoxia-induced factor 1-alpha (HIF-1α) in the blood of children with anemia and chronic kidney disease C1-5 prior to the dialysis and on its background, receiving and not receiving iron preparations and erythropoietin-stimulating drugs to establish the role of HIF-1α in the regulation of erythropoietin synthesis and erythropoiesis. Results. The patients (n=80) with anemia and chronic kidney disease were divided into 3 groups: Group 1: 32 patients with chronic kidney disease C1-5 prior to the dialysis, not receiving therapy; Group 2: 18 patients with chronic kidney disease C2-5 prior to the dialysis, receiving iron-containing preparations and erythropoietin-stimulating drugs; Group 3: 30 patients with chronic kidney disease C3-5 on dialysis, receiving iron preparations and erythropoietin-stimulating drugs. Group 1: we found the increased levels of erythropoietin (28.65 ± 3.66 MIU/ml) and HIF-1α (0.089 ± 0.011 ng/ml; p=0.014 and p=0.005, respectively); Group 2: 63.01 ± 14.84 mIU/ml and 0.138 ± 0.025 ng/ml; p=0.0088 and p=0.005, respectively). Group 3: we found the increased level of HIF-1α (0.098 ± 0.01 ng/ml; p=0.005).Conclusion. An increase in concentration of HIF-1α in children with anemia and chronic kidney disease C1-5 prior and on dialysis receiving and not receiving therapy with iron-containing drugs and erythropoietin-stimulating agents confirms the role of HIF-1α in the regulation of erythropoietin and erythropoiesis synthesis in anemia.
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Chong, Zhao Zhong, Jing-Qiong Kang i Kenneth Maiese. "Hematopoietic Factor Erythropoietin Fosters Neuroprotection through Novel Signal Transduction Cascades". Journal of Cerebral Blood Flow & Metabolism 22, nr 5 (maj 2002): 503–14. http://dx.doi.org/10.1097/00004647-200205000-00001.
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In addition to promoting the survival, proliferation, and differentiation of immature erythroid cells, erythropoietin and the erythropoietin receptor have recently been shown to modulate cellular signal transduction pathways that extend beyond the erythropoietic function of erythropoietin. In particular, erythropoietin has been linked to the prevention of programmed cell death in neuronal systems. Although this work is intriguing, the underlying molecular mechanisms that serve to mediate neuroprotection by erythropoietin are not well understood. Further analysis illustrates that erythropoietin modulates two distinct components of programmed cell death that involve the degradation of DNA and the externalization of cellular membrane phosphatidylserine residues. Initiation of the cascades that modulate protection by erythropoietin and its receptor may begin with the activation of the Janus tyrosine kinase 2 protein. Subsequent downstream mechanisms appear to lead to the activation of multiple signal transduction pathways that include transcription factor STAT5 (signal transducers and activators of transcription), Bcl-2, protein kinase B, cysteine proteases, mitogen-activated protein kinases, proteintyrosine phosphatases, and nuclear factor-κB. New knowledge of the cellular pathways regulated by erythropoietin in neuronal environments will potentially solidify the development and initiation of therapeutic strategies against nervous system disorders.
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Tiwari, Neeraj K., Monica Sathyanesan, Vikas Kumar i Samuel S. Newton. "A Comparative Analysis of Erythropoietin and Carbamoylated Erythropoietin Proteome Profiles". Life 11, nr 4 (19.04.2021): 359. http://dx.doi.org/10.3390/life11040359.
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In recent years, erythropoietin (EPO) has emerged as a useful neuroprotective and neurotrophic molecule that produces antidepressant and cognitive-enhancing effects in psychiatric disorders. However, EPO robustly induces erythropoiesis and elevates red blood cell counts. Chronic administration is therefore likely to increase blood viscosity and produce adverse effects in non-anemic populations. Carbamoylated erythropoietin (CEPO), a chemically engineered modification of EPO, is non-erythropoietic but retains the neurotrophic and neurotrophic activity of EPO. Blood profile analysis after EPO and CEPO administration showed that CEPO has no effect on red blood cell or platelet counts. We conducted an unbiased, quantitative, mass spectrometry-based proteomics study to comparatively investigate EPO and CEPO-induced protein profiles in neuronal phenotype PC12 cells. Bioinformatics enrichment analysis of the protein expression profiles revealed the upregulation of protein functions related to memory formation such as synaptic plasticity, long term potentiation (LTP), neurotransmitter transport, synaptic vesicle priming, and dendritic spine development. The regulated proteins, with roles in LTP and synaptic plasticity, include calcium/calmodulin-dependent protein kinase type 1 (Camk1), Synaptosomal-Associated Protein, 25 kDa (SNAP-25), Sectretogranin-1 (Chgb), Cortactin (Cttn), Elongation initiation factor 3a (Eif3a) and 60S acidic ribosomal protein P2 (Rplp2). We examined the expression of a subset of regulated proteins, Cortactin, Grb2 and Pleiotrophin, by immunofluorescence analysis in the rat brain. Grb2 was increased in the dentate gyrus by EPO and CEPO. Cortactin was induced by CEPO in the molecular layer, and pleiotrophin was increased in the vasculature by EPO. The results of our study shed light on potential mechanisms whereby EPO and CEPO produce cognitive-enhancing effects in clinical and preclinical studies.
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Weiss, Mitchell J., i Camila O. dos Santos. "Chaperoning erythropoiesis". Blood 113, nr 10 (5.03.2009): 2136–44. http://dx.doi.org/10.1182/blood-2008-09-115238.
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AbstractMultisubunit complexes containing molecular chaperones regulate protein production, stability, and degradation in virtually every cell type. We are beginning to recognize how generalized and tissue-specific chaperones regulate specialized aspects of erythropoiesis. For example, chaperones intersect with erythropoietin signaling pathways to protect erythroid precursors against apoptosis. Molecular chaperones also participate in hemoglobin synthesis, both directly and indirectly. Current knowledge in these areas only scratches the surface of what is to be learned. Improved understanding of how molecular chaperones regulate erythropoietic development and hemoglobin homeostasis should identify biochemical pathways amenable to pharmacologic manipulation in a variety of red blood cell disorders including thalassemia and other anemias associated with hemoglobin instability.
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Renner, Wilfried, Melanie Kaiser, Sebastian Khuen, Olivia Trummer, Harald Mangge i Tanja Langsenlehner. "The Erythropoetin rs1617640 Gene Polymorphism Associates with Hemoglobin Levels, Hematocrit and Red Blood Cell Count in Patients with Peripheral Arterial Disease". Genes 11, nr 11 (4.11.2020): 1305. http://dx.doi.org/10.3390/genes11111305.
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Background: Erythropoietin has a pivotal role in erythropoiesis and angiogenesis. A common polymorphism (rs1617640, A > C) in the promoter of the erythropoietin gene (EPO) has been associated with erythropoietin expression and microvascular complications of diabetes. We aimed to analyze the potential role of this polymorphism in the pathogenesis of peripheral arterial disease (PAD). Methods: EPO genotypes and laboratory markers for erythropoiesis were determined in 945 patients with PAD. Results: The minor EPO rs1617640 C-allele was associated in an allele-dose-dependent manner with hemoglobin levels (p = 0.006), hematocrit (p = 0.029), and red blood cell count (p = 0.003). In a multivariate linear regression analysis including conventional risk factors diabetes, sex, and smoking, EPO genotypes were furthermore associated with age at onset of PAD symptoms (p = 0.009). Conclusions: The EPO rs1617640 gene polymorphism affects erythropoiesis, leads to an earlier onset of PAD, and is a potential biomarker for the pathogenesis of this disease.
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Riebandt, G., S. A. South, K. Odunsi, S. Lele i K. Rodabaugh. "Limited value of routine iron studies prior to initiation of erythropoietin therapy in patients with ovarian cancer". Journal of Clinical Oncology 25, nr 18_suppl (20.06.2007): 19677. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.19677.
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19677 Background: Anemia is a common consequence of cancer which significantly impacts patient quality of life. The mainstay of treatment for cancer- and chemotherapy-related anemia is erythropoietin therapy. However, approximately 30% to 50% of patients will not respond to these growth factors. The literature attributes this lack of response to functional iron deficiency, when iron stores are normal but the body cannot meet the increased rate of erythropoiesis. We evaluated the iron status of patients with ovarian malignancies receiving chemotherapy and erythropoietin therapy to establish a baseline for implementation of an intervention service. Methods: After obtaining Institutional Review Board approval, we identified 55 ovarian cancer patients receiving erythropoietin therapy from January to December 2005. We then performed a retrospective chart review for patients who had iron studies available. Results: Thirty-four patients had complete iron studies performed, while an additional 10 had only a ferritin level obtained. The mean hemoglobin for all patients was 9.9g/dl (6.9–13.1) with a mean MCV (mean corpuscular volume) of 92.7fl. Four (12%) patients were iron deficient based on ferritin <100ng/ml and iron saturation <20%. However, these patients had normal MCVs, indicating iron deficiency was not the etiology of their anemia. A few patients were assessed for B12 and folate deficiency, but none were identified. Interestingly, we had 22 patients with elevated ferritin levels (greater than 322ng/ml), with the highest being 2178ng/ml. Conclusions: Our results identified a few patients who were iron deficient, but none were diagnosed with iron deficiency anemia. Therefore, the role of routine iron screening in patients with a normal MCV prior to initiation of erythropoietin therapy is in question. We believe that functional iron deficiency may contribute to anemia in our population. Therefore, we suggest that all patients receive iron supplementation at erythropoietin therapy initiation. We plan to prospectively assess the optimal route of iron administration in ovarian cancer patients in order to improve the response rate to erythropoietic growth factors. No significant financial relationships to disclose.
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Millot, Sarah, Valérie Andrieu, Philippe Letteron, Saïd Lyoumi, Margarita Hurtado-Nedelec, Zoubida Karim, Olivier Thibaudeau i in. "Erythropoietin stimulates spleen BMP4-dependent stress erythropoiesis and partially corrects anemia in a mouse model of generalized inflammation". Blood 116, nr 26 (23.12.2010): 6072–81. http://dx.doi.org/10.1182/blood-2010-04-281840.
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Abstract Mouse bone marrow erythropoiesis is homeostatic, whereas after acute anemia, bone morphogenetic protein 4 (BMP4)–dependent stress erythropoiesis develops in the spleen. The aim of this work was to compare spleen stress erythropoiesis and bone marrow erythropoiesis in a mouse model of zymosan-induced generalized inflammation, which induces long-lasting anemia and to evaluate the ability of erythropoietin (Epo) injections to correct anemia in this setting. The effects of zymosan and/or Epo injections on erythroid precursor maturation and apoptosis, serum interferon-γ levels, hematologic parameters, and spleen BMP4 expression were analyzed, as well as the effect of zymosan on red blood cell half-life. We found that bone marrow erythropoiesis is suppressed by inflammation and does not respond to Epo administration, despite repression of erythroblast apoptosis. On the contrary, a robust erythropoietic response takes place in the spleen after Epo injections in both control and zymosan-induced generalized inflammation mice. This specific response implies Epo-mediated induction of BMP4 expression by F4/80+ spleen macrophages, proliferation of stress burst-forming units-erythroid, and increased number of spleen erythroblasts. It allows only partial recovery of anemia, probably because of peripheral destruction of mature red cells. It is not clear whether similar BMP4-dependent stress erythropoiesis can occur in human bone marrow after Epo injections.
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Ohneda, O., N. Yanai i M. Obinata. "Combined action of c-kit and erythropoietin on erythroid progenitor cells". Development 114, nr 1 (1.01.1992): 245–52. http://dx.doi.org/10.1242/dev.114.1.245.
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Mutations at the murine dominant-white spotting locus (W) (c-kit) affect various aspects of hematopoiesis. We have made antibodies against c-Kit with the synthetic peptides deduced from the murine c-kit gene and examined the role of c-Kit in erythropoiesis. The antibody inhibited the stromal cell-dependent large colony formation of the erythroid progenitors. In the culture of erythropoietin-responsive erythroid progenitors of the anemia-inducing Friend virus-infected mouse spleen, the antibody inhibited only proliferation, but not differentiation of the progenitor cells. The inhibition was effective only at the early phase (within 6 hours after erythropoietin addition) before the cells start to proliferate induced by erythropoietin. During the early phase, erythropoietin down-regulated c-kit gene expression. These results suggest a mechanism of combined action of c-Kit with erythropoietin on the lineage-restricted erythroid progenitor cells.
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Beguin, Y., G. Lipscei, H. Thoumsin i G. Fillet. "Blunted erythropoietin production and decreased erythropoiesis in early pregnancy [see comments]". Blood 78, nr 1 (1.07.1991): 89–93. http://dx.doi.org/10.1182/blood.v78.1.89.89.
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Abstract After decreasing in the first trimester of pregnancy, the total red blood cell mass increases in the second and third trimesters to peak at term at about 120% to 125% of nonpregnant values, but how this is brought about by changes in the rate of erythropoiesis is not known. We evaluated erythropoiesis by measuring serum transferrin receptor (TfR) levels in 406 women during normal pregnancy (N = 317), at delivery (N = 63), or in the early postpartum (N = 27). Despite the presence of the placenta and the frequent occurrence of iron deficiency, TfR levels remained low in the first two trimesters and increased in the third trimester and at delivery. To explain why erythropoiesic activity was relatively low in early pregnancy, we also measured serum immunoreactive erythropoietin (Epo) in relation to the degree of anemia. There was a very strong correlation between serum TfR and Epo levels in the entire group (r = .59, P less than .0001) as well as in each period of pregnancy. Epo levels remained low for the degree of anemia and did not correlate with hematocrit in the first two trimesters, but recovered afterwards. In the early postpartum, Epo production and erythropoiesis were normal. We conclude that: (1) erythropoiesis is decreased in the first part of pregnancy but increases afterwards; and (2) blunted Epo production in early pregnancy could be responsible for that observation.
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Beguin, Y., G. Lipscei, H. Thoumsin i G. Fillet. "Blunted erythropoietin production and decreased erythropoiesis in early pregnancy [see comments]". Blood 78, nr 1 (1.07.1991): 89–93. http://dx.doi.org/10.1182/blood.v78.1.89.bloodjournal78189.
Pełny tekst źródłaStreszczenie:
After decreasing in the first trimester of pregnancy, the total red blood cell mass increases in the second and third trimesters to peak at term at about 120% to 125% of nonpregnant values, but how this is brought about by changes in the rate of erythropoiesis is not known. We evaluated erythropoiesis by measuring serum transferrin receptor (TfR) levels in 406 women during normal pregnancy (N = 317), at delivery (N = 63), or in the early postpartum (N = 27). Despite the presence of the placenta and the frequent occurrence of iron deficiency, TfR levels remained low in the first two trimesters and increased in the third trimester and at delivery. To explain why erythropoiesic activity was relatively low in early pregnancy, we also measured serum immunoreactive erythropoietin (Epo) in relation to the degree of anemia. There was a very strong correlation between serum TfR and Epo levels in the entire group (r = .59, P less than .0001) as well as in each period of pregnancy. Epo levels remained low for the degree of anemia and did not correlate with hematocrit in the first two trimesters, but recovered afterwards. In the early postpartum, Epo production and erythropoiesis were normal. We conclude that: (1) erythropoiesis is decreased in the first part of pregnancy but increases afterwards; and (2) blunted Epo production in early pregnancy could be responsible for that observation.
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Beguin, Yves. "Erythropoiesis and Erythropoietin in Multiple Myeloma". Leukemia & Lymphoma 18, nr 5-6 (styczeń 1995): 413–21. http://dx.doi.org/10.3109/10428199509059639.
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Rossert, Jerome, i Kai-Uwe Eckardt. "Erythropoietin receptors: their role beyond erythropoiesis". Nephrology Dialysis Transplantation 20, nr 6 (19.04.2005): 1025–28. http://dx.doi.org/10.1093/ndt/gfh800.
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Lykov, A. P., M. A. Surovtseva, O. V. Poveshchenko, N. A. Bondarenko, I. I. Kim, A. M. Chernyvski i A. V. Fomichev. "EFFECT OF ERYTHROPOIETIN ON CYTOKINE PRODUCTION BY STEM CELLS". Medical Immunology (Russia) 21, nr 5 (13.12.2019): 861–68. http://dx.doi.org/10.15789/1563-0625-2019-5-861-868.
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Erythropoietin (EPO) is mainly used to stimulate erythropoiesis. Its cytoprotective effects upon other cells of the human body and animals were recently shown, in particular, anti-apoptotic effect was observed. EPO effect upon the cells is mediated by interaction with erythropoietin receptor, with a complex forming a heterodimeric bond with β-common chain (CD131). In the present work, we studied the changes in erythropoietin receptor expression, and production spectrum of biologically active molecules in bone marrow mononuclear cells (BM-MNC) of patients with coronary heart disease. The flow cytometric assays showed that short-term incubation of BM-MNC with erythropoietin caused increased expression of the erythropoietin receptors on hematopoietic stem cells and tended to reduce the number of endothelial progenitor cells carrying the erythropoietin receptors. Solid-phase enzyme immunoassay in conditioned media from BM-MNC revealed that long-term (72 hours) exposure of BM-MNC to erythropoietin promoted increased production of IL-1β, PDGF-AB, and Epo, if compared to the basal production level (p < 0.05). Short-term incubation of BM-MNC with erythropoietin (60 minutes) caused a significant increase in the IL-1β, PDGF-AB and CXCL-12 / SDF-1α production levels, as well as significant reduction in the IL-10 production levels compared to the basal levels (p < 0.05).
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Putri, Rachma Greta Perdana, Amanatus Sholikhah i Novi Sukirto. "Risk Factor for Erythropoietin Resistance in Hemodialysis Patient : Literature Review". Ahmad Dahlan Medical Journal 1, nr 2 (30.11.2020): 33–49. http://dx.doi.org/10.12928/admj.v1i2.3131.
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Anaemia become the complication of chronic kidney disease (CKD) which was caused by decreasing of erythropoietin. Erythropoietin stimulating agent (ESA) therapy is one of therapy to overcome the problem, but until 34% of patients have lack of response to ESA treatment. Anaemia in CKD related to the worsen of the diseases, quality of life, and mortality of patients. Decreasing of the response to erythropoietin need to be evaluated to correct anaemic condition. This review is aim to explain the risk factor for erythropoietin resistance. The literature for this review was collected through PUBMED and google scholar. Erythropoietin is glycoprotein secreted 90% by interstitial cells of kidney and 10% by liver cells. The functions of erythropoietin are stimulate the proliferation and cells differentiation in bone marrow, and enhance erythropoiesis. Renal damage can inhibit the secretion of erythropoietin. In patients with ESA treatment, risk factors for resistance are iron deficiency, inadequate haemodialysis, inflammation, hyperparathyroid, nutrition disturbance, antibody mediated Pure Red Cell Aplastic (PRCA). The risk factor can be influenced by genetic variation. Conclusion of this review, there are several factor that influence the response of erythropoietin in hemodialisa patients. Hence, study related anaemia in CKD need further study to optimalize the treatment.
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Emerson, SG, S. Thomas, JL Ferrara i JL Greenstein. "Developmental regulation of erythropoiesis by hematopoietic growth factors: analysis on populations of BFU-E from bone marrow, peripheral blood, and fetal liver". Blood 74, nr 1 (1.07.1989): 49–55. http://dx.doi.org/10.1182/blood.v74.1.49.49.
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Abstract Fetal hematopoiesis is characterized by expanding erythropoiesis to support a continuously increasing RBC mass. To explore the basis for this anabolic, nonhomeostatic erythropoiesis, the proliferative effect of recombinant hematopoietic growth factors on highly enriched hematopoietic progenitor cells from fetal and adult tissues were compared. Fetal hepatic BFU-E, unlike adult bone marrow (BM) or peripheral blood (PB) BFU-E, were capable of proliferating in response to erythropoietin in the absence of added GM colony-stimulating factor (GM-CSF) or interleukin-3 (IL-3), and erythropoietin (Epo) directly stimulated the expansion of the fetal BFU-E pool in suspension culture. A murine monoclonal antibody (MoAb), Ep 3, was raised against enriched fetal liver progenitor cells, which detected all fetal BFU-E and which reacted with the erythropoietin-responsive, GM-CSF/IL-3-independent fraction of adult BM BFU-E and CFU-E. All adult PB BFU-E were Ep 3- but became Ep 3+ after stimulation with GM-CSF or IL-3. These data indicate that Epo plays a unique role in fetal hepatic erythropoiesis, stimulating proliferation of immature BFU-E in addition to promoting terminal differentiation of later erythroid progenitor cells. In addition, these results demonstrate a MoAb which detects all erythropoietin-responsive progenitor cells and distinguishes the BFU-E compartments in adult BM and PB.