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Results for “Erythroid Precursor Cells”

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PubMed1986

Characterization of the hematopoietic defect in paroxysmal nocturnal hemoglobinuria.

We studied the relationship between paroxysmal nocturnal hemoglobinuria (PNH) and bone marrow failure using in vitro hematopoietic colony culture assays. Most of 17 patients with PNH showed decreased colony formation, by erythroid burst-forming cells (BFU-E) and granulocyte-macrophage colony-forming cells (CFU-C) in methylcellulose, disproportionate to their degree of bone marrow biopsy cellularity. Only a minority of the hematopoietic progenitors were sensitive to complement-mediated lysis in vitro. In contrast, normoblasts from maturing erythroid bursts removed from culture and exposed to acidified serum were sensitive to complement-mediated lysis. The size of bursts and the sensitivity of their progeny correlated strongly, suggesting that the PNH defect was acquired in culture as a function of the generational age of erythroid precursor cells. In addition, BFU-E of PNH patients were very sensitive to 3H-thymidine suicide, in comparison with normal individuals and patients with other hemolytic anemias, indicating that a large proportion of primitive erythroid progenitors in PNH bone marrow were in cell cycle. All of these results imply that acquisition of the PNH defect during erythropoiesis may lead to intramedullary destruction of developing erythroid cells. The increased demand that results on the progenitor pool may lead to stem cell depletion and bone marrow failure.

Adolescent↗

PubMed1971

Erythropoietin effects on fetal mouse erythroid cells. I. Cell population and hemoglobin synthesis.

The effect of the hormone, erythropoietin, on cultures of erythroblasts derived from the livers of fetal C57BL/6J mice was examined. An increase both in the content and in the rate of synthesis of normal adult mouse globin chains was detected in hormone-treated cultures. The rate of protein synthesis by individual erythroblasts does not increase in response to the hormone, whereas the absolute number of hemoglobin-synthesizing cells does increase and accounts for the observed stimulation of hemoglobin synthesis. The principal effect of erythropoietin appears to be upon the population of immature erythroid precursor cells which persists in the presence of the hormone, the cells maintaining their ability to replicate, and their capacity to differentiate into hemoglobinizing erythroblasts. In the absence of hormone, already committed erythroblasts continue their development, but erythropoiesis is not sustained.

Animals↗

PubMed2005

Pure red cell aplasia in a prostate cancer patient treated with leuprolide acetate and chlormadinone acetate.

Pure red cell aplasia (PRCA) is characterized by anemia with reticulocytopenia but with normal leukocyte and platelet counts, and a bone marrow with a selective absence of erythroid precursor cells. Drug-induced PRCA is a rare secondary form of PRCA, and is usually acute and fully reversible by the withdrawal of the causative drugs. We report a rare case of PRCA in a prostate cancer patient treated with combined androgen blockade (CAB) consisted of leuprolide acetate as a luteinizing hormone-releasing hormone agonist and chlormadinone acetate as an antiandrogen. This case demonstrated that these drugs could be a cause of PRCA, and suggests that regular close monitoring for anemia is needed in prostate cancer patients treated with these drugs.

Adenocarcinoma↗

PubMed1985

Interferon-induced aplasia: evidence for T-cell-mediated suppression of hematopoiesis and recovery after treatment with horse antihuman thymocyte globulin.

A severe and persistent pancytopenia occurred in a 42-year-old woman with a non-Hodgkin's lymphoma following a 10-day course of intramuscular human leukocyte alpha interferon (IFN, 9.0 IU/day). Within 2 weeks of IFN, marrow nucleated myeloid and erythroid precursor cells and megakaryocytes were nearly absent and marrow progenitor cells (CFU-E, BFU-E, CFU-GM) were undetectable. Analysis of marrow lymphocytes revealed that nearly 50% of the cells were E-rosette+, T gamma+, OKT8+ (suppressor/cytotoxic) T-and/or Leu 7+ natural killer (NK) lymphocytes and 50% were IgM Kappa, B1+, B-lymphocytes. In vitro erythroid culture studies were consistent with T-cell-mediated suppression of erythropoiesis. After 2 months without improvement on corticosteroid/androgen therapy, a 10-day course of intravenous antithymocyte globulin (ATG) was administered. This was followed by a prompt reticulocytosis and a rise in blood neutrophils. After ATG therapy, there was a sixfold reduction in marrow suppressor cells, loss of in vitro suppressor effects on erythroid progenitor cells, and complete reversal of blood and marrow OKT4/OKT8 (helper/suppressor) ratios. These studies suggest that interferon may suppress hematopoiesis in some patients by activating marrow suppressor T- and/or NK cells. Treatment aimed at reduction of marrow suppressor cells may aid in hematologic recovery without eliminating the infiltrating lymphoma.

Adult↗

PubMed1974

Half-life and rate of synthesis of globin messenger ribonucleic acid. Determination of half-life of messenger ribonucleic acid and its relative synthetic rate in erythroid cells.

The specific radioactivity of mouse globin mRNA in blood reticulocytes was measured after injection of [(3)H]uridine into anaemic mice up to 60h before collection of reticulocytes. From these data, the decay of the acid-soluble nucleotide pool in the marrow and the relative marrow-cell composition it is possible to build models that allow the cell life-times and half-life of mRNA in the erythroid cells of the marrow to be calculated. Best fit of models to these data favour a model with either one or two cell divisions from the onset of mRNA synthesis. The single-cell-division model has cell times of 20, 13 and 7h respectively for the basophilic erythroblast, polychromatophilic erythroblast and reticulocyte. The two-cell-division model has cell times of 12, 12, 12 and 7h for the basophilic erythroblast 1 and 2, polychromatophilic erythroblast and reticulocyte respectively. Both models have an mRNA half-life of 17h and a constant rate of mRNA synthesis until enucleation at the reticulocyte stage, when synthesis stops. A declining rate of mRNA synthesis can be accommodated in a two-cell-division model, when synthesis halves at each cell division and cell times are essentially the same as above, but mRNA half-life is either 9h in the basophilic and polychromatophilic erythroblasts and 17h in the later cells, or 10h in the basophilic erythroblasts and polychromatophilic erythroblasts and 14.5h in later cells. In all cases it is clear that mRNA synthesis occurs over a time-period of only 30-36h and that mRNA cannot be pre-synthesized in precursor erythroid cells.

Anemia↗

PubMedDate not supplied

[Effect of B-cell suppressor factor and erythroblast suppressor factor on the colony-forming capacity of hematopoietic stem cells].

Hemopoietic precursor cloning in healthy donors and patients with lymphoproliferative disorders and its regulation in donors by two novel suppressive factors (BSF and ErSF) are investigated. It is shown that the count of erythroid precursors is increased in peripheral blood of patients with non-Hodgkin's lymphoma in contrast to the count of granulocyte-macrophage precursors. BSF inhibits entirely granulocyte-macrophage, macrophage and erythrocyte colony growth. In contrast, ErSF abrogates selectively erythroid precursor cell proliferation and differentiation. The role of the above factor in normal hemopoiesis inhibition mechanism during lymphoproliferative diseases are discussed.

B-Lymphocytes↗

PubMed1982

Friend erythroleukemia virus complex: role of viral components in modifying erythroid differentiation in mice.

The present study was carried out to determine which component of the polycythemic strain of Friend erythroleukemia virus (FV-P)--Friend helper virus [Friend murine leukemia virus (F-MuLV)] of the replication-defective spleen focus-forming virus (SFFV)--is responsible for inducing erythropoietin-independent erythropoiesis and expansion of the erythroid compartment in infected mice. F-MuLV and SFFV were cloned in SC1 cells to give a cell line 643/22N, which released only F-MuLV and SC204, a nonproducer cell line carrying SFFV. On superinfection with specific helper viruses, SC204 yielded further cell lines, which released SFFV in conjunction with 1) Friend, 2) Moloney, or 3) Gross helper viruses. With the use of an in vitro colony formation assay to monitor erythropoiesis in the bone marrow of inbred DBA/2J mice infected with any of the virus preparations containing SFFV plus helper virus, the erythroid precursor cell population was found to become erythropoietin-independent and amplified; adult mice infected with any of the helper viruses alone did not develop any symptoms of Friend disease. Thus the biologic activity of the FV-P complex was unaffected by replacement of the F-MuLV with an unrelated helper virus (Moloney or Gross). These results indicated that the SFFV component of FV-P is responsible for modifying erythroid differentiation in adult mice.

Animals↗

PubMed1982

A new candidate for the regulation of erythropoiesis. Insulin-like growth factor I.

The effect of pure human insulin-like growth factor I (IGF I) on the colony formation of late stage erythroid precursor cells (CFU-e) from fetal mouse liver and adult bone marrow was studied in a serum-free culture system. We found that IGF I in physiological concentrations stimulated erythroid colony formation. The combined effect of IGF I and erythropoietin was smaller than the sum of their single effects. The number of colonies induced by IGF I was linearly dependent on the number of plated cells. Our results indicate that IGF I is the first clearly defined mitogen that stimulates the late stages of erythroid differentiation independently of erythropoietin.

Animals↗

PubMed1993

Electron microscopic identification of parvovirus virions in erythroid and granulocytic-line cells in a patient with human parvovirus B19 induced pancytopenia.

In this short report we describe a patient with human parvovirus B19 (HPV B19)-induced transient pancytopenia. Parvovirus virions were seen by electron microscopy in both erythroid and granulocytic precursors. Erythroid cells are not the only targets in these cases. We draw attention to this disorder so that physicians involved with hematological disorders and transplantation be more aware of this infection.

Adult↗

PubMed1984

[Development of early erythroid precursors (BFUe) from mouse bone marrow in a serum-free culture media. Effect of hemin].

In culture medium containing albumin, iron saturated transferrin, phospholipids, cholesterol and erythropoietin, BFUe growth requires foetal Calf serum. Without serum the BFUe development is advantageously restored by the addition of hemin associated with spleen conditioned medium. In erythropoietin supplemented serum-free medium the growth of primitive erythroid precursor cells is closely dependent on growth factor supply found in spleen conditioned medium. Using this medium allows us to clearly distinguish between the respective effects of erythropoietin and of BPA on erythroid progenitor cells.

Animals↗

PubMed1979

Regulation of vitamin B6 metabolism in human red cells.

The effects of pyridoxine and pyridoxal 5-phosphate (PLP) administration on pyridoxine kinase (PnK) and asparate aminotransferase (EGOT), a PLP-dependent enzyme, were studied in human red cells separated into young and old populations by density centrifugation. After a delay of 48 hr, both pyridoxine and PLP increase EGOT activity in mature red cells by activating preformed GOT apoenzyme. In addition, in young erythroid cells, pyridoxine therapy induces synthesis of PnK, while both pyridoxine and PLP induce synthesis of GOT apoprotein. Thus, PLP stimulates EGOT induction without a change in PnK activity, suggesting that PLP enters erythroid precursor cells without prior dephosphorylation. However, with both pyridoxine and PLP, the full induction of enzyme activities reflect the gradual replacement of circulating red cells by newly formed cells with higher enzyme levels. Therefore, the use of EGOT as a measure of vitamin B6 nutritional status requires recognition of the complexities of intracellular enzyme regulation.

Alanine Transaminase↗

PubMed2003

Synergistic effect of verotoxin and interferon-alpha on erythropoiesis.

Previous studies have shown that the verotoxin receptor globotriaosyl ceramide is involved in interferon-alpha (IFN-alpha) signaling pathways. The results of the present study indicate that verotoxin used in combination with IFN-alpha had a direct cytotoxic effect on erythrocyte development by targeting nucleated erythrocyte precursors. Toxin treatment alone had no significant effect on erythropoiesis. However, treatment with 100 ng/ml of verotoxin (VT) in combination with 100 U/ml of IFN-alpha was highly cytotoxic (>90%) to erythroid cells in human cord blood cultures by day 14 post-treatment. The lack of effect on other hematopoietic cells, and the relatively modest decrease in the number of erythroid colonies formed (28%) as a result of IFN-alpha/VT treatment, indicate that the cytotoxicity was targeted specifically toward cells committed to the erythrocyte lineage. IFN-alpha treatment alone did not result in cytotoxicity or a significant reduction in the number of erythroid colonies formed. However, IFN-alpha treatment did result in an increase in the surface expression of verotoxin receptors as determined by flow cytometry following labeling of cells with VT-FITC. Abnormalities in erythrocyte morphology and anemia are associated with infection by verotoxin-producing Escherichia coli such as serotype O157:H7. These symptoms are frequently attributed to passage of erythrocytes through partially occluded blood vessels following toxin-induced damage to endothelial cells. The present results document a synergistic cytotoxic effect of IFN-alpha and verotoxin on erythropoiesis, which could have relevance to clinical infection with verotoxin-producing bacteria.

Drug Synergism↗

PubMed1997

Genetics of erythropoiesis: induced mutations in mice and zebrafish.

Production of red blood cells (erythropoiesis) in the vertebrate embryo is critical to its survival and subsequent development. As red cells are the first blood cells to appear in embryogenesis, their origin reflects commitment of mesoderm to an hematopoietic fate and provides an avenue by which to examine the development of the hematopoietic system, including the hematopoietic stem cell (HSC). We discuss the genetics of erythropoiesis as studied in two systems: the mouse and zebrafish (Danio rerio). In the mouse, targeted disruption has established several genes as essential at different stages of hematopoiesis or erythroid precursor cell maturation. In the zebrafish, numerous mutants displaying a wide range of phenotypes have been isolated, although the affected genes are unknown. In comparing mouse knockout and zebrafish mutant phenotypes, we propose a pathway for erythropoiesis that emphasizes the apparent similarity of the mutants and the complementary nature of investigation in the two species. We speculate that further genetic studies in mouse and zebrafish will identify the majority of essential genes and define a regulatory network for hematopoiesis in vertebrates.

Animals↗

PubMed2002

Early-stage idiopathic (primary) myelofibrosis--current issues of diagnostic features.

Idiopathic myelofibrosis (IMF) is generally characterized by bone marrow (BM) fibrosis, anemia, splenomegaly and a leuko-erythroblastic blood picture. Although, histopathology is in keeping with the assumption of a stepwise evolution of the disease, little hematological data are available for patients with prefibrotic and early stages of disease. Therefore a clinicopathological study was performed that included firstly an exploratory sample of 68 patients with minor supportive therapy in whom BM biopsies during follow-up (41 +/- 32 months) revealed an evolution of a prefibrotic or very early fibrotic lesion into overt IMF. The validation sample consisted of 556 patients with pretreatment marrow specimens on admission. Diagnostic features and BM lesions were identical compared with the patients of the exploratory sample at their first examination. BM biopsies were processed by routine stainings including silver impregnation (reticulin fibers) and frequently also by immunohistochemistry to identify megakaryocytes and erythroid precursor cells more properly. Apart from minor hemorrhage and peripheral thrombosis patients with early stage IMF presented with non-specific symptoms including varying degrees of leukocytosis (51%), anemia (38%), a platelet count exceeding 600 x 10(9)/l (86%), splenomegaly (15%) and increase in leukocyte alkaline phosphatase (LAP) (24%) and serum lactate dehydrogenase (LDH) (20%). BM histology confirmed a moderate increase in hematopoiesis with a mixed granulocytic and megakaryocytic myeloproliferation, a reduction of erythroid precursors and significant megakaryocytic abnormalities. In keeping with the first BM examination of the exploratory sample no or only a borderline to slight increase in reticulin fibers was detectable, however, in 68 of 134 patients follow-up biopsies revealed a transition into overt IMF (intervals about three years). Median survival of this cohort with early-stage IMF was 129 months thus contrasting manifest IMF with an usually more unfavorable prognosis. Recognition of early stage IMF certainly alters the generally applied diagnostic criteria of this disorder. Regarding patients with associated thrombocytosis, differentiation from essential thrombocythemia is recommended. Moreover, characterization of early stage IMF probably exerts an impact on survival and may influence the decision to perform a BM transplantation.

Adult↗

PubMed1989

Evidence for an elevated frequency of in vivo somatic cell mutations in ataxia telangiectasia.

Somatic cell mutation frequency in vivo was measured in individuals with high cancer risk who were from ataxia telangiectasia (A-T) families. The assay for somatic mutation measures the frequency of variant erythrocytes which are progeny of erythroid precursor cells with mutations that result in a loss of gene expression at the polymorphic glycophorin A (GPA) locus. Samples from 14 of 15 A-T homozygotes showed high frequencies of GPA gene expression-loss variant cells with normal expression of only one of the two alleles at the GPA locus (i.e., GPA hemizygous variant cells). The mean elevation of the frequency of hemizygous variant cells over those in normal controls and unaffected family members was 7-14-fold. A-T homozygotes also showed an increase in the frequency of cells in which one allele at the GPA locus had lost expression and in which the remaining allele was expressed at a homozygous level (i.e., GPA homozygous variant cells). Family members who are obligate A-T heterozygotes did not appear to have a significantly elevated frequency of GPA hemizygous or homozygous variant cells. These indications of elevated in vivo frequencies of variant erythrocytes in A-T homozygotes support a causal link between susceptibility to somatic mutation and susceptibility to cancer.

Adult↗

PubMed1987

Inhibition by interleukin-1 of the action of erythropoietin on erythroid precursors and its possible role in the pathogenesis of hypoplastic anaemias.

Highly purified and cloned preparations of interleukin-1 (IL-1) were found to antagonize the capacity of erythropoietin (Epo) to stimulate the proliferation of mouse spleen and bone marrow erythroid precursor cells (EPC) in culture. Cloned murine IL-1 and purified and cloned human IL-1 alpha and IL-1 beta were approximately equipotent in this assay. IL-1 inhibited the proliferation response of EPC even when added as long as 17 h after Epo, suggesting that IL-1 does not affect binding of Epo to receptors or biochemical events following shortly thereafter. Indomethacin did not influence the inhibitory effect of IL-1 on Epo-induced proliferation, and PGE2 had no demonstrable effect on the process. Tumor-necrosis factor-alpha and interferons beta 1, and gamma did not affect Epo-induced proliferation. It is suggested that IL-1 mediated antagonism of the effects of Epo on erythroid precursors is a factor in the pathogenesis of many types of hypoplastic anaemia, including those associated with infections, rheumatoid arthritis and systemic lupus erythematosus, giant-cell arteritis, graft-versus-host disease and disorders associated with lymphocyte-mediated suppression of erythropoiesis.

Anemia↗

PubMed1985

Cell lineage heterogeneity in blast crisis of chronic myeloid leukaemia.

Blast cells from 45 patients with chronic myeloid leukaemia in blast crisis (CML-BC) were immunologically phenotyped with a panel of 26 monoclonal antibodies and studied for terminal deoxynucleotidyl transferase (TdT) content. Out of 45 blast-populations, 28 showed a myeloid, 14 a lymphoid, two a mixed and one an unclassifiable marker profile. In contrast to acute myeloid leukaemia (AML), we found frequent involvement of the thrombopoietic and erythropoietic systems in myeloid CML-BC. Furthermore, the marker profile on blast cells in myeloid CML-BC was different from that seen in AML. The blast cells in lymphoid blast crises of CML displayed the same lymphoid marker profile as those in acute lymphoblastic leukaemia. In three of 16 patients who were serially tested, we observed phenotypic changes in the blast cell populations. In one patient the blasts changed from lymphoid to myeloid type while remaining TdT-positive; in another case the blasts switched from granulomonocytic TdT-negative to granulomonocytic TdT-positive. In the third patient erythroid precursor cells appeared as the disease progressed. The results indicate the capacity of blast populations in CML-patients during blast crisis to differentiate along several pathways.

Adolescent↗

PubMed2005

Bone marrow changes in chronic myelogenous leukaemia after long-term treatment with the tyrosine kinase inhibitor STI571: an immunohistochemical study on 75 patients.

AIMS: To carry out an immunohistochemical study on bone marrow (BM) biopsy specimens in 75 patients with chronic myelogenous leukaemia (CML) on long-term STI571 therapy. METHODS AND RESULTS: Sequential BM specimens taken at intervals of 21 +/- 6 months were investigated by enzyme- and immunohistochemistry including proliferating cell nuclear antigen and apoptosis. Evaluation was performed either by semiquantitative scoring or by morphometry (CD61+ megakaryopoiesis). In 41 patients with chronic phase CML, treatment resulted in a significant decrease in cellularity and neutrophil granulopoiesis contrasting with an accumulation of erythroid precursor cells. Morphometry showed a reduction of abnormal micromegakaryocytes consistent with normalization. Regression of myelofibrosis was identified in eight of 15 patients, whereas progression occurred in 17 patients; mostly in those with acceleration and blastic crisis. The increased post-treatment incidence of reactive lymphoid nodules was remarkable. Myeloblasts, CD34+ progenitors and immature myelomonocytic cells initially decreased, but recurred in 14 patients who later developed a relapse. STI571 exerted an inhibitory effect on cell proliferation associated with enhanced apoptosis in responding patients. CONCLUSION: Long-term treatment with STI571 exerts pronounced changes on BM histopathology that not only involve haematopoiesis and stromal constituents, but also proliferation and apoptosis.

Antigens, CD34↗