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Journal articles on the topic 'BFU-E (Burst Forming Unit Erythroid)'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Royet, J., G. Mouchiroud, S. Arnaud, T. Oddos, S. Galland, and JP Blanchet. "Kidney cell lysates contain an activity that stimulates mature erythroid burst-forming-unit (mBFU-E) proliferation." Blood 76, no. 10 (1990): 1965–71. http://dx.doi.org/10.1182/blood.v76.10.1965.1965.

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Abstract This study reports the detection of an activity that stimulates the development of a subclass of burst-forming unit-erythroid (BFU-E) progenitors giving rise to small bursts in semi-solid cultures established in the presence of saturating concentrations of erythropoietin. These progenitors are considered to be mature BFU-E. The activity is found in extracts from kidney cells and appears to be physiologically regulated as it was respectively enhanced and decreased in kidneys from anemic and polycythemic mice. The disappearance of activity in kidney-cell extracts during long-term polycy

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2

Royet, J., G. Mouchiroud, S. Arnaud, T. Oddos, S. Galland, and JP Blanchet. "Kidney cell lysates contain an activity that stimulates mature erythroid burst-forming-unit (mBFU-E) proliferation." Blood 76, no. 10 (1990): 1965–71. http://dx.doi.org/10.1182/blood.v76.10.1965.bloodjournal76101965.

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This study reports the detection of an activity that stimulates the development of a subclass of burst-forming unit-erythroid (BFU-E) progenitors giving rise to small bursts in semi-solid cultures established in the presence of saturating concentrations of erythropoietin. These progenitors are considered to be mature BFU-E. The activity is found in extracts from kidney cells and appears to be physiologically regulated as it was respectively enhanced and decreased in kidneys from anemic and polycythemic mice. The disappearance of activity in kidney-cell extracts during long-term polycythemia co

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3

DeZern, Amy E., Michael A. McDevitt, Richard J. Jones, and Robert A. Brodsky. "Burst-Forming Unit-Erythroid Assays (BFU-E) Can Help Distinguish Cellular Bone Marrow Failure Disorders." Blood 120, no. 21 (2012): 3475. http://dx.doi.org/10.1182/blood.v120.21.3475.3475.

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Abstract Abstract 3475 Cytopenias in the context of cellular marrows cause significant morbidity for patients and are challenging for clinicians to diagnose and treat. Often the differential diagnosis includes pure red cell aplasia (PRCA), large granular lymphocyte leukemia (LGL), marrow suppression associated with systemic inflammation, and clonal bone marrow failure disorders such as myelodysplastic syndrome (MDS) or paroxysmal nocturnal hemoglobinuria (PNH). Unfortunately, it can be difficult to differentiate between these possibilities, and correct treatment depends on accurate diagnosis.

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4

Aucella, F. "Desferrioxamine improves burst-forming unit-erythroid (BFU-E) proliferation in haemodialysis patients." Nephrology Dialysis Transplantation 13, no. 5 (1998): 1194–99. http://dx.doi.org/10.1093/ndt/13.5.1194.

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5

Rich, IN. "The effect of 5-fluorouracil on erythropoiesis." Blood 77, no. 6 (1991): 1164–70. http://dx.doi.org/10.1182/blood.v77.6.1164.1164.

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Abstract The effects of a single dose (150 mg/kg) of 5-fluorouracil on mature erythroid and erythropoietic and multipotential in vitro precursor populations in the bone marrow and spleen and circulating biologically (erythroid colony forming unit [CFU-E] assay) and immunologically active (enzyme-linked immunosorbent assay) erythropoietin (Epo) are described. All mature erythroid (reticulocytes, erythrocytes) and in vitro erythropoietic precursors (CFU-E, erythroid burst-forming unit [BFU-E]) are severely reduced, if not eradicated. Transient repopulation of the pure BFU-E and CFU-E populations

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6

Rich, IN. "The effect of 5-fluorouracil on erythropoiesis." Blood 77, no. 6 (1991): 1164–70. http://dx.doi.org/10.1182/blood.v77.6.1164.bloodjournal7761164.

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The effects of a single dose (150 mg/kg) of 5-fluorouracil on mature erythroid and erythropoietic and multipotential in vitro precursor populations in the bone marrow and spleen and circulating biologically (erythroid colony forming unit [CFU-E] assay) and immunologically active (enzyme-linked immunosorbent assay) erythropoietin (Epo) are described. All mature erythroid (reticulocytes, erythrocytes) and in vitro erythropoietic precursors (CFU-E, erythroid burst-forming unit [BFU-E]) are severely reduced, if not eradicated. Transient repopulation of the pure BFU-E and CFU-E populations on days

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7

Dai, CH, SB Krantz, and KM Zsebo. "Human burst-forming units-erythroid need direct interaction with stem cell factor for further development." Blood 78, no. 10 (1991): 2493–97. http://dx.doi.org/10.1182/blood.v78.10.2493.2493.

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Abstract To understand the factors that regulate the early growth and development of immature erythroid progenitor cells, the burst-forming units-erythroid (BFU-E), it is necessary to have both highly purified target cells and a medium free of serum. When highly purified human blood BFU-E were cultured in a serum-free medium adequate for the growth of later erythroid progenitors, BFU-E would not grow even with the addition of recombinant human interleukin-3 (rIL-3), known to be essential for these cells. However, the addition of recombinant human stem cell factor (rSCF), which supports germ ce

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8

Dai, CH, SB Krantz, and KM Zsebo. "Human burst-forming units-erythroid need direct interaction with stem cell factor for further development." Blood 78, no. 10 (1991): 2493–97. http://dx.doi.org/10.1182/blood.v78.10.2493.bloodjournal78102493.

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To understand the factors that regulate the early growth and development of immature erythroid progenitor cells, the burst-forming units-erythroid (BFU-E), it is necessary to have both highly purified target cells and a medium free of serum. When highly purified human blood BFU-E were cultured in a serum-free medium adequate for the growth of later erythroid progenitors, BFU-E would not grow even with the addition of recombinant human interleukin-3 (rIL-3), known to be essential for these cells. However, the addition of recombinant human stem cell factor (rSCF), which supports germ cell and pl

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9

Flygare, Johan, Violeta Rayon Estrada, Chanseok Shin, Sumeet Gupta та Harvey F. Lodish. "HIF1α synergizes with glucocorticoids to promote BFU-E progenitor self-renewal". Blood 117, № 12 (2011): 3435–44. http://dx.doi.org/10.1182/blood-2010-07-295550.

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AbstractWith the aim of finding small molecules that stimulate erythropoiesis earlier than erythropoietin and that enhance erythroid colony-forming unit (CFU-E) production, we studied the mechanism by which glucocorticoids increase CFU-E formation. Using erythroid burst-forming unit (BFU-E) and CFU-E progenitors purified by a new technique, we demonstrate that glucocorticoids stimulate the earliest (BFU-E) progenitors to undergo limited self-renewal, which increases formation of CFU-E cells > 20-fold. Interestingly, glucocorticoids induce expression of genes in BFU-E cells that contain prom

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10

Suzuki, Norio, Naruyoshi Suwabe, Osamu Ohneda, et al. "Identification and characterization of 2 types of erythroid progenitors that express GATA-1 at distinct levels." Blood 102, no. 10 (2003): 3575–83. http://dx.doi.org/10.1182/blood-2003-04-1154.

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AbstractTranscription factor GATA-1 is essential for the development of the erythroid lineage. To ascertain whether strict control of GATA-1 expression level is necessary for achieving proper erythropoiesis, we established transgenic mouse lines expressing green fluorescent protein (GFP) under the control of the GATA-1 gene hematopoietic regulatory domain. We examined the GATA-1 expression level by exploiting the transgenic mice and found 2 GFP-positive hematopoietic progenitor fractions in the bone marrow. One is the GFPhigh fraction containing mainly CFU-E and proerythroblasts, which coexpre

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11

Pistoia, V., R. Ghio, A. Nocera, A. Leprini, A. Perata, and M. Ferrarini. "Large granular lymphocytes have a promoting activity on human peripheral blood erythroid burst-forming units." Blood 65, no. 2 (1985): 464–72. http://dx.doi.org/10.1182/blood.v65.2.464.464.

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Abstract Peripheral blood mononuclear cells were fractionated according to the expression of a variety of surface markers, and the fractions obtained were tested for erythroid burst-forming unit (BFU-E) colony formation. BFU-Es were detected in the HLA-DR+ non-T cell fraction, but gave rise to optimum colony numbers only in the presence of a nonadherent, relatively radioresistant cell. This accessory cell was found among the HLA-DR- non-T, non-B cells, a fraction that was particularly enriched in large granular lymphocytes (LGLs). Experiments carried out to assess directly the surface markers

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12

Pistoia, V., R. Ghio, A. Nocera, A. Leprini, A. Perata, and M. Ferrarini. "Large granular lymphocytes have a promoting activity on human peripheral blood erythroid burst-forming units." Blood 65, no. 2 (1985): 464–72. http://dx.doi.org/10.1182/blood.v65.2.464.bloodjournal652464.

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Peripheral blood mononuclear cells were fractionated according to the expression of a variety of surface markers, and the fractions obtained were tested for erythroid burst-forming unit (BFU-E) colony formation. BFU-Es were detected in the HLA-DR+ non-T cell fraction, but gave rise to optimum colony numbers only in the presence of a nonadherent, relatively radioresistant cell. This accessory cell was found among the HLA-DR- non-T, non-B cells, a fraction that was particularly enriched in large granular lymphocytes (LGLs). Experiments carried out to assess directly the surface markers of the ac

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13

Broudy, VC, N. Lin, M. Brice, B. Nakamoto, and T. Papayannopoulou. "Erythropoietin receptor characteristics on primary human erythroid cells." Blood 77, no. 12 (1991): 2583–90. http://dx.doi.org/10.1182/blood.v77.12.2583.2583.

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Abstract Erythropoietin (EP) exerts its effects on erythropoiesis by binding to a cell surface receptor. We examined EP receptor expression during normal human erythroid differentiation and maturation from the burst- forming unit-erythroid (BFU-E) to the reticulocyte level. In contrast to previous studies, we assessed EP receptor number and affinity in erythroid precursors immunologically purified from fresh bone marrow aspirates or fetal liver samples and in reticulocytes purified from peripheral blood. EP receptors were quantitated by equilibrium binding experiments with 125I EP. We found th

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14

Broudy, VC, N. Lin, M. Brice, B. Nakamoto, and T. Papayannopoulou. "Erythropoietin receptor characteristics on primary human erythroid cells." Blood 77, no. 12 (1991): 2583–90. http://dx.doi.org/10.1182/blood.v77.12.2583.bloodjournal77122583.

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Erythropoietin (EP) exerts its effects on erythropoiesis by binding to a cell surface receptor. We examined EP receptor expression during normal human erythroid differentiation and maturation from the burst- forming unit-erythroid (BFU-E) to the reticulocyte level. In contrast to previous studies, we assessed EP receptor number and affinity in erythroid precursors immunologically purified from fresh bone marrow aspirates or fetal liver samples and in reticulocytes purified from peripheral blood. EP receptors were quantitated by equilibrium binding experiments with 125I EP. We found that purifi

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15

Stopka, T., J. H. Zivny, P. Stopkova, J. F. Prchal, and J. T. Prchal. "Human Hematopoietic Progenitors Express Erythropoietin." Blood 91, no. 10 (1998): 3766–72. http://dx.doi.org/10.1182/blood.v91.10.3766.3766_3766_3772.

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Erythropoietin (EPO) is a factor essential for erythroid cell proliferation, differentiation, and survival. The production of EPO by the kidneys in response to hypoxia and anemia is well documented. To determine whether EPO is also produced by hematopoietic cells, we analyzed the expression of EPO in normal human hematopoietic progenitors and in their progeny. Undifferentiated CD34+lin− hematopoietic progenitors do not have detectable EPO mRNA. Differentiating CD34+ cells that are stimulated with recombinant human EPO in serum-free liquid cultures express both EPO and EPO receptor (EPOR). Beca

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16

Brashem-Stein, C., DA Flowers, FO Smith, SJ Staats, RG Andrews, and ID Bernstein. "Ontogeny of hematopoietic stem cell development: reciprocal expression of CD33 and a novel molecule by maturing myeloid and erythroid progenitors." Blood 82, no. 3 (1993): 792–99. http://dx.doi.org/10.1182/blood.v82.3.792.792.

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Abstract We have identified a molecule expressed by human marrow granulocyte/monocyte colony-forming cells (CFU-GM), erythroid colony- forming cells (CFU-E), and erythroid burst-forming units (BFU-E), but not their precursors detectable in long-term bone marrow culture. This antigen, detected by flow microfluorimetry using monoclonal antibody 7B9, is coexpressed with CD33 on many CD34+ CFCs, although only the 7B9 antigen was detected on a portion of BFU-E and CFU-E, whereas only CD33 was found on a portion of CFU-GM. Antibody 7B9 appears to be useful for isolating subsets of progenitors based

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17

Brashem-Stein, C., DA Flowers, FO Smith, SJ Staats, RG Andrews, and ID Bernstein. "Ontogeny of hematopoietic stem cell development: reciprocal expression of CD33 and a novel molecule by maturing myeloid and erythroid progenitors." Blood 82, no. 3 (1993): 792–99. http://dx.doi.org/10.1182/blood.v82.3.792.bloodjournal823792.

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We have identified a molecule expressed by human marrow granulocyte/monocyte colony-forming cells (CFU-GM), erythroid colony- forming cells (CFU-E), and erythroid burst-forming units (BFU-E), but not their precursors detectable in long-term bone marrow culture. This antigen, detected by flow microfluorimetry using monoclonal antibody 7B9, is coexpressed with CD33 on many CD34+ CFCs, although only the 7B9 antigen was detected on a portion of BFU-E and CFU-E, whereas only CD33 was found on a portion of CFU-GM. Antibody 7B9 appears to be useful for isolating subsets of progenitors based on their

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18

Takahashi, T., K. Ozawa, K. Takahashi, S. Asano, and F. Takaku. "Susceptibility of human erythropoietic cells to B19 parvovirus in vitro increases with differentiation." Blood 75, no. 3 (1990): 603–10. http://dx.doi.org/10.1182/blood.v75.3.603.603.

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Abstract B19 human parvovirus is the etiologic agent of transient aplastic crisis. To better understand B19 virus-induced hematopoietic suppression, we studied the host cell range of the virus using in vitro bone marrow cultures. First, B19 virus replication was examined in the presence of various purified cytokines using DNA dot blot analysis. Replication was detected only in erythropoietin-containing cultures. The other cytokines (granulocyte/macrophage colony-stimulating factor [GM-CSF], G-CSF, M-CSF, interleukin-1 [IL-1], IL-2, IL-3, and IL-6) did not support virus replication, indicating

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19

Takahashi, T., K. Ozawa, K. Takahashi, S. Asano, and F. Takaku. "Susceptibility of human erythropoietic cells to B19 parvovirus in vitro increases with differentiation." Blood 75, no. 3 (1990): 603–10. http://dx.doi.org/10.1182/blood.v75.3.603.bloodjournal753603.

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B19 human parvovirus is the etiologic agent of transient aplastic crisis. To better understand B19 virus-induced hematopoietic suppression, we studied the host cell range of the virus using in vitro bone marrow cultures. First, B19 virus replication was examined in the presence of various purified cytokines using DNA dot blot analysis. Replication was detected only in erythropoietin-containing cultures. The other cytokines (granulocyte/macrophage colony-stimulating factor [GM-CSF], G-CSF, M-CSF, interleukin-1 [IL-1], IL-2, IL-3, and IL-6) did not support virus replication, indicating the restr

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20

Abkowitz, JL, KM Sabo, B. Nakamoto, et al. "Diamond-blackfan anemia: in vitro response of erythroid progenitors to the ligand for c-kit." Blood 78, no. 9 (1991): 2198–202. http://dx.doi.org/10.1182/blood.v78.9.2198.2198.

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Abstract To provide insights into the pathogenesis of Diamond-Blackfan anemia, we examined the in vitro response of erythroid progenitors to the recently isolated ligand for c-kit (stem cell factor, SCF). For these studies, marrow or blood mononuclear cells from 10 Diamond-Blackfan patients were cultured with erythropoietin (Ep), Ep and interleukin-3, Ep and granulocyte-macrophage colony-stimulating factor, or Ep and lymphocyte conditioned media (LCM). These combinations were tested in the presence or absence of SCF. The mean number of cells per erythroid burst increased 5 to 50-fold in cultur

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21

Abkowitz, JL, KM Sabo, B. Nakamoto, et al. "Diamond-blackfan anemia: in vitro response of erythroid progenitors to the ligand for c-kit." Blood 78, no. 9 (1991): 2198–202. http://dx.doi.org/10.1182/blood.v78.9.2198.bloodjournal7892198.

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To provide insights into the pathogenesis of Diamond-Blackfan anemia, we examined the in vitro response of erythroid progenitors to the recently isolated ligand for c-kit (stem cell factor, SCF). For these studies, marrow or blood mononuclear cells from 10 Diamond-Blackfan patients were cultured with erythropoietin (Ep), Ep and interleukin-3, Ep and granulocyte-macrophage colony-stimulating factor, or Ep and lymphocyte conditioned media (LCM). These combinations were tested in the presence or absence of SCF. The mean number of cells per erythroid burst increased 5 to 50-fold in cultures contai

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22

Tsai, S., V. Patel, E. Beaumont, HF Lodish, DG Nathan, and CA Sieff. "Differential binding of erythroid and myeloid progenitors to fibroblasts and fibronectin." Blood 69, no. 6 (1987): 1587–94. http://dx.doi.org/10.1182/blood.v69.6.1587.1587.

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Abstract Using a novel coverslip-transfer culture technique, we recently demonstrated that primitive erythroid burst-forming units (BFU-E) can migrate, proliferate, and differentiate in intimate association with stromal fibroblastoid cells in the presence of serum proteins and erythropoietin. No other exogenous hemopoietic growth factors are required. Most of the colonies that develop in this system are very large erythroid bursts, and very few granulocyte-macrophage (GM) colonies are observed. In this report, we present data indicating that the predominance of erythroid burst colonies in this

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23

Tsai, S., V. Patel, E. Beaumont, HF Lodish, DG Nathan, and CA Sieff. "Differential binding of erythroid and myeloid progenitors to fibroblasts and fibronectin." Blood 69, no. 6 (1987): 1587–94. http://dx.doi.org/10.1182/blood.v69.6.1587.bloodjournal6961587.

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Using a novel coverslip-transfer culture technique, we recently demonstrated that primitive erythroid burst-forming units (BFU-E) can migrate, proliferate, and differentiate in intimate association with stromal fibroblastoid cells in the presence of serum proteins and erythropoietin. No other exogenous hemopoietic growth factors are required. Most of the colonies that develop in this system are very large erythroid bursts, and very few granulocyte-macrophage (GM) colonies are observed. In this report, we present data indicating that the predominance of erythroid burst colonies in this culture

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24

Mizuguchi, T., M. Kosaka, and S. Saito. "Activin A suppresses proliferation of interleukin-3-responsive granulocyte-macrophage colony-forming progenitors and stimulates proliferation and differentiation of interleukin-3-responsive erythroid burst-forming progenitors in the peripheral blood." Blood 81, no. 11 (1993): 2891–97. http://dx.doi.org/10.1182/blood.v81.11.2891.bloodjournal81112891.

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We examined the effects of activin A on the proliferation and differentiation of immature hematopoietic progenitors prepared from peripheral blood (PB) using methylcellulose and liquid-suspension culture. In a kinetic analysis, colony formation by PB granulocyte- macrophage colony-forming unit (CFU-GM) was delayed in a dose-dependent manner by the addition of activin A only when stimulated with interleukin-3 (IL-3), but not when stimulated with granulocyte colony- stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), or stem cell factor (SCF) plus G-CSF. DNA-sy

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25

Stopka, T., J. H. Zivny, P. Stopkova, J. F. Prchal, and J. T. Prchal. "Human Hematopoietic Progenitors Express Erythropoietin." Blood 91, no. 10 (1998): 3766–72. http://dx.doi.org/10.1182/blood.v91.10.3766.

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Abstract Erythropoietin (EPO) is a factor essential for erythroid cell proliferation, differentiation, and survival. The production of EPO by the kidneys in response to hypoxia and anemia is well documented. To determine whether EPO is also produced by hematopoietic cells, we analyzed the expression of EPO in normal human hematopoietic progenitors and in their progeny. Undifferentiated CD34+lin− hematopoietic progenitors do not have detectable EPO mRNA. Differentiating CD34+ cells that are stimulated with recombinant human EPO in serum-free liquid cultures express both EPO and EPO receptor (EP

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26

Gambone, Julia E., Stephanie S. Dusaban, Roxana Loperena, Yuji Nakata, and Susan E. Shetzline. "The c-Myb target gene neuromedin U functions as a novel cofactor during the early stages of erythropoiesis." Blood 117, no. 21 (2011): 5733–43. http://dx.doi.org/10.1182/blood-2009-09-242131.

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Abstract The requirement of c-Myb during erythropoiesis spurred an interest in identifying c-Myb target genes that are important for erythroid development. Here, we determined that the neuropeptide neuromedin U (NmU) is a c-Myb target gene. Silencing NmU, c-myb, or NmU's cognate receptor NMUR1 expression in human CD34+ cells impaired burst-forming unit-erythroid (BFU-E) and colony-forming unit-erythroid (CFU-E) formation compared with control. Exogenous addition of NmU peptide to NmU or c-myb siRNA-treated CD34+ cells rescued BFU-E and yielded a greater number of CFU-E than observed with contr

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27

Bhagia, Pooja, Narla Mohandas, and Xiuli An. "Isolation and Functional Characterization of Human Erythroid Progenitors: BFU-E and CFU-E." Blood 118, no. 21 (2011): 1028. http://dx.doi.org/10.1182/blood.v118.21.1028.1028.

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Abstract Abstract 1028 The two committed erythroid progenitor populations that have been functionally defined by colony assays are burst-forming unit-erythroid (BFU-E) and colony-forming unit-erythroid (CFU-E). While significant progress has been made in defining these two progenitor populations in the murine system, their characterization in the human system is incomplete. To address this issue, we have characterized the dynamic changes in surface expression levels of number of proteins including CD34, c-kit, IL-3R, CD36, CD71, GPA and CD45 during proliferation of purified human CD34+ cells f

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28

Mizuguchi, T., M. Kosaka, and S. Saito. "Activin A suppresses proliferation of interleukin-3-responsive granulocyte-macrophage colony-forming progenitors and stimulates proliferation and differentiation of interleukin-3-responsive erythroid burst-forming progenitors in the peripheral blood." Blood 81, no. 11 (1993): 2891–97. http://dx.doi.org/10.1182/blood.v81.11.2891.2891.

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Abstract We examined the effects of activin A on the proliferation and differentiation of immature hematopoietic progenitors prepared from peripheral blood (PB) using methylcellulose and liquid-suspension culture. In a kinetic analysis, colony formation by PB granulocyte- macrophage colony-forming unit (CFU-GM) was delayed in a dose-dependent manner by the addition of activin A only when stimulated with interleukin-3 (IL-3), but not when stimulated with granulocyte colony- stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), or stem cell factor (SCF) plus G-CS

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29

Sonoda, Y., YC Yang, GG Wong, SC Clark, and M. Ogawa. "Erythroid burst-promoting activity of purified recombinant human GM-CSF and interleukin-3: studies with anti-GM-CSF and anti-IL-3 sera and studies in serum-free cultures." Blood 72, no. 4 (1988): 1381–86. http://dx.doi.org/10.1182/blood.v72.4.1381.1381.

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Abstract We studied the erythroid burst-promoting activity (BPA) of recombinant human granulocyte/macrophage colony-stimulating factor (GM-CSF) and Interleukin-3 (IL-3) with two experimental approaches. First we studied the effects of polyclonal antisera prepared against human GM-CSF and gibbon IL-3 on colony formation from 1,000 bone marrow null cells/dish in serum-containing culture. Both GM-CSF and IL-3 independently enhanced erythroid burst formation; however, IL-3 showed more BPA activity than GM-CSF. These data are in agreement with an emerging view that the primary targets of IL-3 are p

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30

Sonoda, Y., YC Yang, GG Wong, SC Clark, and M. Ogawa. "Erythroid burst-promoting activity of purified recombinant human GM-CSF and interleukin-3: studies with anti-GM-CSF and anti-IL-3 sera and studies in serum-free cultures." Blood 72, no. 4 (1988): 1381–86. http://dx.doi.org/10.1182/blood.v72.4.1381.bloodjournal7241381.

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We studied the erythroid burst-promoting activity (BPA) of recombinant human granulocyte/macrophage colony-stimulating factor (GM-CSF) and Interleukin-3 (IL-3) with two experimental approaches. First we studied the effects of polyclonal antisera prepared against human GM-CSF and gibbon IL-3 on colony formation from 1,000 bone marrow null cells/dish in serum-containing culture. Both GM-CSF and IL-3 independently enhanced erythroid burst formation; however, IL-3 showed more BPA activity than GM-CSF. These data are in agreement with an emerging view that the primary targets of IL-3 are primitive

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31

Dybedal, I., and SE Jacobsen. "Transforming growth factor beta (TGF-beta), a potent inhibitor of erythropoiesis: neutralizing TGF-beta antibodies show erythropoietin as a potent stimulator of murine burst-forming unit erythroid colony formation in the absence of a burst-promoting activity." Blood 86, no. 3 (1995): 949–57. http://dx.doi.org/10.1182/blood.v86.3.949.949.

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Abstract Transforming growth factor beta (TGF-beta) is a bifunctional regulator of the growth of myeloid progenitors and is here demonstrated to directly inhibit the growth of primitive erythroid progenitors by 95% to 100% regardless of the cytokines stimulating growth. Autocrine TGF- beta production of primitive hematopoietic progenitors has previously been reported. In the present study, a neutralizing TGF-beta antibody (anti-TGF-beta) added to serum-containing cultures, resulted in a 3-, 4- , and 25-fold increase in burst-forming unit erythroid (BFU-E) colony formation in response to interl

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32

Dybedal, I., and SE Jacobsen. "Transforming growth factor beta (TGF-beta), a potent inhibitor of erythropoiesis: neutralizing TGF-beta antibodies show erythropoietin as a potent stimulator of murine burst-forming unit erythroid colony formation in the absence of a burst-promoting activity." Blood 86, no. 3 (1995): 949–57. http://dx.doi.org/10.1182/blood.v86.3.949.bloodjournal863949.

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Transforming growth factor beta (TGF-beta) is a bifunctional regulator of the growth of myeloid progenitors and is here demonstrated to directly inhibit the growth of primitive erythroid progenitors by 95% to 100% regardless of the cytokines stimulating growth. Autocrine TGF- beta production of primitive hematopoietic progenitors has previously been reported. In the present study, a neutralizing TGF-beta antibody (anti-TGF-beta) added to serum-containing cultures, resulted in a 3-, 4- , and 25-fold increase in burst-forming unit erythroid (BFU-E) colony formation in response to interleukin-4 (

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33

De Feo, T. M., M. D. Cappellini, and G. Fiorelli. "Effect of estrogens and progesterone on human peripheral erythroid burst-forming unit (BFU-E) growth." American Journal of Hematology 38, no. 2 (1991): 81–85. http://dx.doi.org/10.1002/ajh.2830380202.

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34

Umemura, Tsukuru, Kenichi Umene, Junji Nishimura, Yasuyuki Fukumaki, Yoshiyuki Sakaki, and Hiroshi Ibayashi. "Expression of c-myc oncogene during differentiation of human burst-forming unit, erythroid (BFU-E)." Biochemical and Biophysical Research Communications 135, no. 2 (1986): 521–26. http://dx.doi.org/10.1016/0006-291x(86)90025-2.

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35

Goltry, Kristin L., and Vikram P. Patel. "Specific Domains of Fibronectin Mediate Adhesion and Migration of Early Murine Erythroid Progenitors." Blood 90, no. 1 (1997): 138–47. http://dx.doi.org/10.1182/blood.v90.1.138.

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Abstract The binding of late stage erythroid cells to fibronectin (FN) has been well characterized and is believed to be critical for the terminal stages of erythroid differentiation, but the adhesive properties of more primitive murine erythroid progenitors and the role of these interactions during earlier stages of erythropoiesis has not been determined. Using chymotryptic fragments and inhibitory probes, we have tested the ability of each of the major cell binding domains of FN; the RGDS sequence, the CS-1 sequence, and the carboxy-terminal heparin-binding domain (HBD), to promote adhesion

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36

Goltry, Kristin L., and Vikram P. Patel. "Specific Domains of Fibronectin Mediate Adhesion and Migration of Early Murine Erythroid Progenitors." Blood 90, no. 1 (1997): 138–47. http://dx.doi.org/10.1182/blood.v90.1.138.138_138_147.

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The binding of late stage erythroid cells to fibronectin (FN) has been well characterized and is believed to be critical for the terminal stages of erythroid differentiation, but the adhesive properties of more primitive murine erythroid progenitors and the role of these interactions during earlier stages of erythropoiesis has not been determined. Using chymotryptic fragments and inhibitory probes, we have tested the ability of each of the major cell binding domains of FN; the RGDS sequence, the CS-1 sequence, and the carboxy-terminal heparin-binding domain (HBD), to promote adhesion of primit

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37

Dainiak, N., D. Sutter, and S. Kreczko. "L-triiodothyronine augments erythropoietic growth factor release from peripheral blood and bone marrow leukocytes." Blood 68, no. 6 (1986): 1289–97. http://dx.doi.org/10.1182/blood.v68.6.1289.1289.

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Abstract To investigate cellular mechanisms involved in thyroid hormone stimulation of erythropoiesis, we studied the response of erythroid burst-forming unit (BFU-E) proliferation to L-triiodothyronine (L-T3) in a serum-free culture system. When added directly to culture, L-T3 stimulates erythroid burst formation by normal human bone marrow cells. In contrast, granulocyte-macrophage colony formation is unaffected. Enhancement of erythroid burst formation by L-T3 required the presence of nylon wool adherent and/or B-4 antigen-positive light-density marrow populations. Addition of other erythro

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38

Dainiak, N., D. Sutter, and S. Kreczko. "L-triiodothyronine augments erythropoietic growth factor release from peripheral blood and bone marrow leukocytes." Blood 68, no. 6 (1986): 1289–97. http://dx.doi.org/10.1182/blood.v68.6.1289.bloodjournal6861289.

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To investigate cellular mechanisms involved in thyroid hormone stimulation of erythropoiesis, we studied the response of erythroid burst-forming unit (BFU-E) proliferation to L-triiodothyronine (L-T3) in a serum-free culture system. When added directly to culture, L-T3 stimulates erythroid burst formation by normal human bone marrow cells. In contrast, granulocyte-macrophage colony formation is unaffected. Enhancement of erythroid burst formation by L-T3 required the presence of nylon wool adherent and/or B-4 antigen-positive light-density marrow populations. Addition of other erythropoietic f

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39

Wisniewski, D., A. Strife, M. Wachter, and B. Clarkson. "Regulation of human peripheral blood erythroid burst-forming unit growth by T lymphocytes and T lymphocyte subpopulations defined by OKT4 and OKT8 monoclonal antibodies." Blood 65, no. 2 (1985): 456–63. http://dx.doi.org/10.1182/blood.v65.2.456.bloodjournal652456.

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To reexamine the influence that T lymphocytes have on the regulation of human peripheral blood burst-forming unit (BFU-E) proliferation in the absence of a statistically significant number of monocytes, very low numbers (3 to 10 X 10(3)/mL) of a null cell fraction highly enriched for BFU-E were cultured alone and in the presence of 5 X 10(5) sheep erythrocyte-purified, autologous T lymphocytes in a methylcellulose culture system containing erythropoietin. T lymphocytes consistently enhanced the growth of BFU-E from the null cell fraction, as reflected in both their number and size. Irradiation

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40

Aulova, Kseniya S., Andrey E. Urusov, Ludmila B. Toporkova, et al. "Production of Abzymes in Th, CBA, and C57BL/6 Mice before and after MOG Treatment: Comparing Changes in Cell Differentiation and Proliferation." Biomolecules 10, no. 1 (2019): 53. http://dx.doi.org/10.3390/biom10010053.

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Till yet there is no data concerning mechanisms of autoimmune diseases development. Experimental autoimmune encephalomyelitis (EAE) prone C57BL/6 (T- and B-lymphocyte response), non-autoimmune CBA, and Th mice with T cell response were immunized with myelin oligodendrocyte glycoprotein (MOG35–55) to compare different characteristics of autoimmune reaction development. Bone marrow differentiation profiles of hematopoietic stem cells (HSCs), lymphocyte proliferation in various organs associated with the production of antibodies against DNA, myelin basic protein (MBP), and MOG, as well as abzymes

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Huddleston, Hannah, Bailin Tan, Feng-Chun Yang та ін. "Functional p85α gene is required for normal murine fetal erythropoiesis". Blood 102, № 1 (2003): 142–45. http://dx.doi.org/10.1182/blood-2002-10-3245.

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Abstract In vitro studies suggest that activation of class IA phosphatidylinositol 3 (PI-3) kinase is necessary for normal erythroid cell development. However, when class IA PI-3 kinase–deficient mice were generated by a targeted deletion of the p85α regulatory subunit, fetal erythropoiesis was reportedly unaffected. Given the discrepancies between these studies, we performed a more detailed in vivo analysis of class IA PI-3 kinase–deficient embryos. Day-14.5 p85α-/- embryos are pale with a marked reduction of mature erythrocytes in their peripheral blood. Further, the absolute number and freq

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Khalaf, Waleed F., Hilary White, Mary Jo Wenning, Attilio Orazi, Reuben Kapur, and David A. Ingram. "K-Ras is essential for normal fetal liver erythropoiesis." Blood 105, no. 9 (2005): 3538–41. http://dx.doi.org/10.1182/blood-2004-05-2021.

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AbstractIn vitro studies suggest that Ras activation is necessary for erythroid cell development. However, genetic inactivation of the Ras isoforms H-Ras, N-Ras, and K-Ras in mice reportedly did not affect adult or fetal erythropoiesis, though K-Ras-/- embryos were anemic. Given these discrepancies, we performed a more detailed analysis of fetal erythropoiesis in K-Ras-/- embryos. Day-13.5 K-Ras-/- embryos were pale with a marked reduction of mature erythrocytes in their fetal livers. The frequency and number of both early (erythroid burst-forming unit [BFU-E]) and late erythroid progenitors (

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43

Inada, Tomohisa, Atsushi Iwama, Seiji Sakano, Mitsuharu Ohno, Ken-ichi Sawada, and Toshio Suda. "Selective Expression of the Receptor Tyrosine Kinase, HTK, on Human Erythroid Progenitor Cells." Blood 89, no. 8 (1997): 2757–65. http://dx.doi.org/10.1182/blood.v89.8.2757.

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Abstract HTK is a receptor tyrosine kinase of the Eph family. To characterize the involvement of HTK in hematopoiesis, we generated monoclonal antibodies against HTK and investigated its expression on human bone marrow cells. About 5% of the bone marrow cells were HTK+, which were also c-Kit+, CD34low, and glycophorin A−/low. Assays of progenitors showed that HTK+c-Kit+ cells consisted exclusively of erythroid progenitors, whereas HTK−c-Kit+ cells contained progenitors of granulocytes and macrophages as well as those of erythroid cells. Most of the HTK+ erythroid progenitors were stem cell fac

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44

Trivedi, Gaurang, Daichi Inoue, Cynthia Chen, et al. "Muscarinic acetylcholine receptor regulates self-renewal of early erythroid progenitors." Science Translational Medicine 11, no. 511 (2019): eaaw3781. http://dx.doi.org/10.1126/scitranslmed.aaw3781.

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Adult stem and progenitor cells are uniquely capable of self-renewal, and targeting this process represents a potential therapeutic opportunity. The early erythroid progenitor, burst-forming unit erythroid (BFU-E), has substantial self-renewal potential and serves as a key cell type for the treatment of anemias. However, our understanding of mechanisms underlying BFU-E self-renewal is extremely limited. Here, we found that the muscarinic acetylcholine receptor, cholinergic receptor, muscarinic 4 (CHRM4), pathway regulates BFU-E self-renewal and that pharmacological inhibition of CHRM4 corrects

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45

Perdahl, EB, BL Naprstek, WC Wallace, and JM Lipton. "Erythroid failure in Diamond-Blackfan anemia is characterized by apoptosis." Blood 83, no. 3 (1994): 645–50. http://dx.doi.org/10.1182/blood.v83.3.645.645.

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Abstract Programmed cell death, also known as apoptosis, is frequently initiated when cells are deprived of specific trophic factors. To investigate if accelerated apoptosis contributes to the pathogenesis of Diamond- Blackfan anemia (DBA), a rare pure red blood cell aplasia of childhood, we studied the effect of erythropoietin (epo) deprivation on erythroid progenitors and precursors from the bone marrow of DBA patients as compared with hematologically normal controls. Apoptosis in response to epo deprivation was evaluated by enumeration of colony-forming unit- erythroid (CFU-E)- and burst-fo

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46

Perdahl, EB, BL Naprstek, WC Wallace, and JM Lipton. "Erythroid failure in Diamond-Blackfan anemia is characterized by apoptosis." Blood 83, no. 3 (1994): 645–50. http://dx.doi.org/10.1182/blood.v83.3.645.bloodjournal833645.

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Programmed cell death, also known as apoptosis, is frequently initiated when cells are deprived of specific trophic factors. To investigate if accelerated apoptosis contributes to the pathogenesis of Diamond- Blackfan anemia (DBA), a rare pure red blood cell aplasia of childhood, we studied the effect of erythropoietin (epo) deprivation on erythroid progenitors and precursors from the bone marrow of DBA patients as compared with hematologically normal controls. Apoptosis in response to epo deprivation was evaluated by enumeration of colony-forming unit- erythroid (CFU-E)- and burst-forming uni

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47

Wisniewski, D., A. Strife, M. Wachter, and B. Clarkson. "Regulation of human peripheral blood erythroid burst-forming unit growth by T lymphocytes and T lymphocyte subpopulations defined by OKT4 and OKT8 monoclonal antibodies." Blood 65, no. 2 (1985): 456–63. http://dx.doi.org/10.1182/blood.v65.2.456.456.

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Abstract:

Abstract To reexamine the influence that T lymphocytes have on the regulation of human peripheral blood burst-forming unit (BFU-E) proliferation in the absence of a statistically significant number of monocytes, very low numbers (3 to 10 X 10(3)/mL) of a null cell fraction highly enriched for BFU-E were cultured alone and in the presence of 5 X 10(5) sheep erythrocyte-purified, autologous T lymphocytes in a methylcellulose culture system containing erythropoietin. T lymphocytes consistently enhanced the growth of BFU-E from the null cell fraction, as reflected in both their number and size. Ir

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48

Alter, BP, ME Knobloch, and RS Weinberg. "Erythropoiesis in Fanconi's anemia." Blood 78, no. 3 (1991): 602–8. http://dx.doi.org/10.1182/blood.v78.3.602.602.

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Abstract Fanconi's anemia (FA) is an autosomal recessive condition in which greater than 90% of the homozygotes develop aplastic anemia. To determine the relation between erythroid progenitors and clinical status, blood and marrow mononuclear cells were cultured in methyl cellulose with erythropoietin, plus other hematopoietic growth factors, and growth in normal oxygen (20%) was compared with growth in low, physiologic oxygen (5%). Peripheral blood cultures were performed from 24 patients, and marrows from six. Patients were classified into six clinical groups. Group 1: Severe aplasia, transf

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49

Alter, BP, ME Knobloch, and RS Weinberg. "Erythropoiesis in Fanconi's anemia." Blood 78, no. 3 (1991): 602–8. http://dx.doi.org/10.1182/blood.v78.3.602.bloodjournal783602.

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Fanconi's anemia (FA) is an autosomal recessive condition in which greater than 90% of the homozygotes develop aplastic anemia. To determine the relation between erythroid progenitors and clinical status, blood and marrow mononuclear cells were cultured in methyl cellulose with erythropoietin, plus other hematopoietic growth factors, and growth in normal oxygen (20%) was compared with growth in low, physiologic oxygen (5%). Peripheral blood cultures were performed from 24 patients, and marrows from six. Patients were classified into six clinical groups. Group 1: Severe aplasia, transfused; one

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50

Dainiak, N., G. Warren, D. Sutter, S. Kreczko, and D. Howard. "A monoclonal antibody to exfoliated surface vesicles that recognizes a membrane-associated erythroid burst-promoting activity." Blood 72, no. 3 (1988): 989–94. http://dx.doi.org/10.1182/blood.v72.3.989.bloodjournal723989.

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A monoclonal antibody (MoAb) recognizing a membrane-associated erythroid burst-promoting factor was prepared by immunizing BALB/c mice with plasma membrane-derived vesicles exfoliated from lymphocytes under serum-free conditions. Hybrids secreting antibody reactive with lymphocyte plasma membranes were formally cloned and IgG was purified from monoclonal supernatants or from BALB/c mouse ascites fluid. Two clones (D3-E4 and D3-G9) were found to suppress burst forming unit- erythroid (BFU-E) proliferation when added directly to serum-free human marrow culture. Inhibition to a level of 100% was

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