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PubMed1997

Mpl ligand (MGDF) alone and in combination with stem cell factor (SCF) promotes proliferation and survival of human megakaryocyte, erythroid and granulocyte/macrophage progenitors.

We examined cytokine-stimulated proliferation and survival of human megakaryocyte progenitor cells. We used a reliable, immunoenzymatic method of labeling CD41a-, CD42b-stained megakaryocytes in intact agar cultures to specifically identify and enumerate all megakaryocyte-containing colonies. We examined a previously defined population of cells enriched for megakaryocyte progenitors that coexpress CD34 and the megakaryocyte/platelet marker CD61. These CD34+61+ cells displayed clonogenicity of approximately 30% and contained myeloid, erythroid and megakaryocyte progenitor cells. With single CD34+61+ cells, megakaryocyte growth and development factor ([MGDF], also known as mpl-ligand or thrombopoietin) stimulated 9% of cells to complete their first cell division by day 2 (versus 21% with stem cell factor [SCF], or 13% with interleukin 3 alone). MGDF showed an additive effect with SCF and interleukin 3 to increase this number at least twofold. In purified CD34+61+ cells, MGDF stimulated the survival of megakaryocyte-colony forming cells (CFC) when addition of other proliferative factors was delayed for 5, 10 and 15 days (all p < 0.0001 versus saline control). MGDF also promoted survival of BFU-E and granulocyte-macrophage-CFC for at least 10 days (p < or = 0.0013 and p < or = 0.0362, respectively). SCF alone prolonged survival of CD34+61+ progenitor cells, however, MGDF + SCF was significantly more active. Whereas the action of MGDF on megakaryocyte-CFC was evident both in stimulating proliferation and survival, its ability to promote survival was between two- and fivefold greater than its action to stimulate proliferation. Thus MGDF alone, and in combination with SCF, was active in promoting the survival and proliferation of human progenitor cells of multiple hemopoietic lineages.

Antigens, CD↗
PubMed1998

Impaired activation and binding of the erythropoietin receptor by a mutant gp55 of Friend spleen focus-forming virus, which has a cytoplasmic domain.

A murine erythroleukemogenic retrovirus, Friend spleen focus-forming virus, encodes an envelope protein-like membrane glycoprotein (gp55) in its defective env gene which is responsible for activation of the erythropoietin receptor (EpoR) and the abnormally rapid proliferation of erythroid precursor cells. The S34 mutant gp55, which possesses an additional cytoplasmic domain, is nonpathogenic and its processing to the cell surface is severely reduced compared to that of the wild-type gp55. In this study, we found that the S34 mutant gp55 neither binds to nor activates the EpoR. The S34 mutant gp55 formed disulfide-bonded homodimers in the rough endoplasmic reticulum (RER) membrane much less efficiently than the wild-type gp55, which is consistent with the proposal that homodimer formation is a prerequisite for gp55 to be exported from the RER. We found that the wild-type gp55 that is bound to EpoR in the RER consists of a large number of monomers and a small number of dimers, suggesting that monomers of the S34 mutant gp55 have lost the ability to bind to the EpoR. The 1-bp insertion present in the wild-type gp55 gene, causing a loss of the cytoplasmic domain, is essential for pathogenicity in that it renders the encoded protein capable of both binding to the EpoR and transport to the cell surface.

Animals↗
PubMed1983

Role and induction of 2,3-bisphosphoglycerate synthase.

2,3-Bisphosphoglycerate accumulates in mammalian erythrocytes, where it facilitates the supply of oxygen to the tissues by binding to hemoglobin. Regulatory properties of 2,3-bisphosphoglycerate synthase and phosphatase are discussed. The 2,3-bisphosphoglycerate concentration was shown to rise linearly along with the hemoglobin level during erythroid differentiation. The accumulation of 2,3-bisphosphoglycerate was primarily attributable to an increase in 2,3-bisphosphoglycerate synthase. Antibody-binding studies showed that the increased activity is achieved solely through an increase in the amount of enzyme. It was shown that 2,3-bisphosphoglycerate synthase was synthesized in nucleated erythroid precursor cells and also in anucleated reticulocytes. The mRNA of this protein appears to be fairly stable in reticulocytes. Coordinate expression of hemoglobin and 2,3-bisphosphoglycerate synthase was found during dimethylsulfoxide-induced differentiation of Friend erythroleukemia cells. 2,3-Bisphosphoglycerate rose concomitantly.

2,3-Diphosphoglycerate↗
PubMed1986

Measurements of the frequency of human erythrocytes with gene expression loss phenotypes at the glycophorin A locus.

An assay method is described for determining the frequency of human erythrocytes having a gene expression loss phenotype at the glycophorin A locus presumably due to in vivo somatic mutational events in erythroid precursor cells. Monoclonal antibodies specific for the M and N glycophorin A alleles are used to identify variant cells that lack the expression of one allele in blood samples from MN heterozygotes. Flow cytometry and sorting are used to enumerate and purify variant cells. Using three different antibody combinations which are sensitive to the loss of either the M or the N allele, we find that variant cells occur at a frequency of 1 X 10(-5) in normal donors. We also detect variant cells with an apparent homozygous phenotype suggesting that events leading to homozygosity may occur at similar frequencies to gene loss events. Significant increases in variant cell frequency are observed in cancer patients after exposure to mutagenic chemotherapy drugs.

Adult↗
PubMed1983

Postnatal changes in canine erythrocyte pyruvate kinase isozymes.

The isozyme pattern of pyruvate kinase in canine erythrocytes changes following birth. These changes have been followed by electrophoretic, immunologic, and kinetic measurements of the isozymes. At birth, a mixture of isozymes is present consisting of the M2 isozyme and hybrid molecules containing M2 and R subunits. With increasing animal age, the content of M2 subunits decreases and the content of R subunits increases. At 6 months of age, the isozyme pattern is indistinguishable from that of adult erythrocytes which contain only the R tetramer. We conclude that there is a switch in erythrocyte pyruvate kinase gene expression during the first 6 months of postnatural life. The existence of hybrid molecules during the switch indicates that both M2 and R genes are expressed within each erythroid precursor cell. The developmental changes in erythrocyte pyruvate kinase are consistent with the role of this enzyme in the regulation of the oxygen-transport function of canine hemoglobin by 2,3-diphosphoglycerate in the postnatal period.

2,3-Diphosphoglycerate↗
PubMed1993

Direct effects of 13-cis and all-trans retinoic acid on normal bone marrow (BM) progenitors: comparative study on BM mononuclear cells and on isolated CD34+ BM cells.

The effects of both 13-cis-and all-trans retinoic acid (RA) on colony formation of normal bone marrow (BM) progenitors were investigated in semi-solid (methylcellulose) assays, using either isolated CD34+ cells or BM mononuclear cells. Single cell liquid cultures were performed to further discriminate between direct and indirect effects. RA action results in significant decrease of colony forming units (CFUs). This effect is more pronounced starting from CD34+ progenitors than starting from total BM. This overall decrease in CFUs is due to selective inhibition of CFU-M (macrophage) and erythroid colonies (BFU-E). At the single cell level the CFU-M inhibition is confirmed with--in addition--a significant inhibition of CFU-GM (granulocyte-macrophage) and a marked stimulation of CFU-G (granulocyte)s. Both retinoids exert the above-mentioned effects. All-trans RA, however, is effective at a tenfold lower concentration (10(-7)M) than 13-cis RA (10(-6)M). Results on CD34+ BM fractions (substantially reduced in accessory cells) demonstrate that the described effects can probably be attributed to the direct action of RA on these progenitors; single progenitor (CD34+) cell liquid cultures further prove this point.

Antigens, CD↗
PubMed1992

Iron stores and serum transferrin receptor levels during recombinant human erythropoietin treatment of anemia in rheumatoid arthritis.

Ten rheumatoid arthritis (RA) patients with anemia of chronic disorders (ACD) were treated with recombinant human erythropoietin (r-Hu-Epo) using a dose of 250 U/kg s.c. 3 times a week for 6 weeks, in order to evaluate its effects on the anemia, iron stores, and serum-soluble transferrin receptor (sTfR) levels. All patients showed a rise in hemoglobin (Hb). Median Hb increased from 5.9 (5.5-7.0) at baseline to 6.7 (5.8-7.8) at 3 weeks and to 7.2 (5.9-8.5) mmol/l at 6 weeks during treatment. Ferritin levels decreased significantly during the 6 weeks, and five patients were iron deficient after 6 weeks of treatment. TfR levels increased significantly at 3 and 6 weeks during treatment. These preliminary findings may indicate that r-Hu-Epo is effective in improving ACD in RA. The sTfR rise may be explained by an increase in erythroid precursor cell mass or increased TfR expression and a decrease in tissue iron stores, although direct effects of Epo on TfR regulation cannot be excluded. Large double-blind studies with r-Hu-Epo in patients with RA and ACD are warranted.

Aged↗
PubMed1998

The making of an erythroid cell. Molecular control of hematopoiesis.

The number of circulating red cells is regulated by the daily balance between two processes: the destruction of the old red cells in the liver and the generation of new cells in the bone marrow. The process during which hematopoietic stem cells generate new red cells is called erythropoiesis. This manuscript will describe the molecular mechanisms involved in the process of erythroid differentiation as we understand them today. In particular it will review how erythroid specific growth factor-receptor interactions activate specific transcription factors to turn on the expression of the genes responsible for the establishment of the erythroid phenotype.

Animals↗
PubMed1990

In situ hybridization for the detection of human parvovirus B19 nucleic acid sequences in paraffin-embedded specimens.

Parvovirus infection of pregnant women leading to a transplacentar infection of the fetus may result in hydrops fetalis, and ultimately in intrauterine death of the fetus. In situ hybridization with a biotinylated as well as with a 35S-labeled probe for human parvovirus B19 was performed on formalin-fixed paraffin-embedded (FFPE) tissue from a fetus suffering from non-immunologic hydrops fetalis. Histology was suggestive of viral infection probably with human parvovirus. Parvovirus DNA could be detected and precisely localized mainly in the nuclei of erythroid precursors cells within fetal blood vessels of all organs examined. There was no detection of B19 nucleic acid in parenchymal cells of the placenta or the fetal organs, nor within maternal blood cells. These findings are in agreement with the well-known properties of animal parvoviruses to replicate exclusively in proliferating cells. Taking into consideration the problems in diagnosing human parvovirus infection by light microscopy, we conclude that in situ hybridization with an appropriate non-radioactive probe is a valuable, rapid and safe complementary detection method for the diagnosis and study of human parvovirus infections. The 35S-labeled probe is more sensitive than the biotinylated probe, but has the disadvantages of lower resolution of the signal, longer duration of the assay, the hazard of radioactivity and the shorter shelf-life of the probe.

Adult↗
PubMed2003

Erythropoietin exerts neuroprotection after acute spinal cord injury in rats: effect on lipid peroxidation and early ultrastructural findings.

Lipid peroxidation has been reported to play an important role in spinal cord injury (SCI). Erythropoietin (EPO) is a hematopoietic growth factor that stimulates proliferation and differentiation of erythroid precursor cells and is also known to exert neurotrophic activity in the central nervous system. The purpose of this study was to investigate the effectiveness of recombinant human EPO in attenuating the severity of experimental SCI. Rats were divided into seven groups. Controls (1) received only laminectomy. The trauma-only group (2) underwent 50-g/cm contusion injury and had no medication. In group 3, 30 mg/kg of methylprednisolone was introduced. The vehicle group (4) received vehicle solution containing human serum albumin, which is a solvent of EPO. Groups 5, 6, and 7 received 100 IU/kg, 1,000 IU/kg, and 5,000 IU/kg of EPO, respectively. All treatments were given as single doses, intraperitoneally, immediately after injury. Thiobarbituric acid-reactive substances were estimated to demonstrate lipid peroxidation, and ultrastructure was evaluated by electron microscopy. The results showed that lipid peroxidation by-products increased after injury. Administration of EPO and methylprednisolone sodium succinate (MPSS) reduced thiobarbituric acid-reactive substances after trauma. The best biochemical results were obtained with 5,000 IU/kg of EPO. Electron microscopic findings showed that EPO protected the spinal cord from injury. Although 1,000 IU/kg and 5,000 IU/kg of EPO inhibited lipid peroxidation better than MPSS, ultrastructural neuroprotection was similar.

Acute Disease↗
PubMed1982

The erythrocyte anion transport protein is contranslationally inserted into microsomes.

The biosynthesis of the erythrocyte anion transport protein, Band III (molecular weight 100,000), is of interest, as its NH2-terminal half is hydrophilic and faces the cytoplasmic surface, and its COOH-terminal half spans the phospholipid bilayer several times. To investigate the problem of insertion of Band III into membranes, we used erythroid precursor cells from the spleens of anemic mice as a source of messenger RNA for in vitro studies in the wheat germ and reticulocyte lysate cell-free system containing dog pancreatic microsomes. Immediately after synthesis, Band III was found to be inserted into intracellular membranes in its mature configuration, with the NH2-terminal portion exposed to the cytoplasm and its hydrophobic COOH-terminal portion spanning the lipid bilayer. The newly synthesized Band III was provided with a high mannose asparagine-linked oligosaccharide, which was sensitive to cleavage by endoglycosidase H; this is presumably the precursor of the very large and complex oligosaccharide found on the finished molecule. Band III was found to insert into dog pancreatic microsomes in a cotranslational manner; in synchronized translation studies microsomes could be added as late as the time when the hydrophilic NH2-terminal half of the protein had been synthesized and still allow normal transmembrane insertion and glycosylation. There is no cleavage of any NH2-terminal peptide during membrane insertion. The results suggest that Band III contains a sequence near the middle of the protein that directs its insertions into endoplasmic reticulum membranes.

Animals↗
PubMed1993

Suramin prevents transcription of dorsal marker genes in Xenopus laevis embryos, isolated dorsal blastopore lips and activin A induced animal caps.

Suramin, a polyanionic compound which is known to interact with the receptors of growth factors inhibits the expression of dorsal marker genes in whole embryos and isolated dorsal blastopore lips. Suramin also prevents activin A induced dorsalization of animal cap explants from blastula stage embryos, but it simultaneously evokes a shift of the differentiation pattern from dorsal mesodermal structures (notochord, somites) to ventral mesodermal derivatives (mesothelium and erythroid precursor cells). The results are consistent with the assumption that the dorsal vegetal zone (Nieuwkoop center) primarily releases more general/ventral mesodermalization signals. They further suggest a dual role of activin A in early embryogenesis. While the maternal component may contribute to a more general/ventral type of induction, increasing concentrations of the zygotic component along with the activation of primary response genes may contribute to the dorsalization of the organizer.

Activins↗
PubMed2006

Isolation of erythroid cells from the mouse embryonic yolk sac by laser capture microdissection and subsequent microarray hybridization.

Erythropoietic tissues are complex, containing both erythroid and other cells. The embryonic yolk sac in particular contains primitive erythroid cells in low abundance. Laser capture microdissection (LCM) was performed to isolate erythroid cells, and epithelial cells, from mouse embryonic day 10 (E10) yolk sac. Quantitative RT-PCR was performed to confirm that enriched cell populations were obtained. epsilony- and betaH1-globin mRNAs were enriched in the erythroid compared to the epithelial fraction, and villin mRNA was enriched in the epithelial compared to the erythroid fraction. RNA isolated from the microdissected erythroid cells was of high quality as indicated by capillary electrophoresis. The RNA from the LCM erythroid fraction was linearly amplified with T7 RNA polymerase and hybridized to a Mouse 430A 2.0 Affymetrix array. Forty-eight percent of genes were present in the microarray assays, including low abundance transcripts such as erythroid transcription factors and enzymes involved in heme synthesis. With the LCM/microarray strategy, it will be possible to identify genes that are differentially regulated in native primitive and definitive erythroid cells.

Animals↗
PubMed2006

Effects of human yolk sac endothelial cells on supporting expansion of hematopoietic stem/progenitor cells from cord blood.

In order to investigate the effects of human yolk sac-derived endothelial cells (hYSECs) on the expansion of human hematopoietic stem/progenitor cells (HS/PCs) from umbilical cord blood (UCB) in vitro, we purified hYSEC-like cells from 4-5 week human yolk sacs, which were morphologically similar to endothelial cells and expressed CD31, CD144 and vWF characteristics of endothelial cells. Then we isolated CD34(+) cells from UCB in culture under three different conditions: with hematopoietic cytokines (CKs), contact-coculture or noncontact-coculture with hYSECs supplemented with CKs, and found that the contact-coculture system had the strongest expansion efficiency in the total cells' (TCs) ability to form HPP-CFCs. Erythroid burst-forming units (BFU-E) increased 52.35-fold, 20.26-fold and 27.77-fold, respectively, compared with pre-expansion. We detected that the mRNA of Notch ligands such as Jagged1, Delta1 and Delta4 could express in hYSECs after contacted culture with UCB-CD34(+) cells but not the noncontacted cells by RT-PCR analysis. Therefore, we concluded that the contact-coculture system supplemented with CKs could support the expansion of UCB-HS/PCs in vitro, especially high potential proliferative colony-forming cells (HPP-CFC) and BFU-E, perhaps owing to Notch signal pathway.

Antigens, CD34↗
PubMed2005

Renal anemia aggravated by long-term parvovirus B19 and cytomegalovirus infection in a renal transplant patient: case report and evaluation of B19 seroprevalence in dialysis patients.

Due to viral replication in erythroid precursor cells, severe anemia represents a major complication of B19 infection. However, cytomegalovirus (CMV) is the leading cause of virus-induced complications with a significant impact on graft outcome of renal transplant patients. Herein, we present a long-term B19 infection in a 45-year-old female renal transplant patient, which aggravated the renal anemia associated with a concomitant CMV infection. Since no data were available on the seroprevalence of this virus in pretransplant patients, we determined the B19 serostatus of 90 dialyzed pretransplant adult subjects.

Adult↗
PubMed2001

Lipoxygenase mRNA silencing in erythroid differentiation: The 3'UTR regulatory complex controls 60S ribosomal subunit joining.

15-lipoxygenase (LOX) expression is translationally silenced in early erythroid precursor cells by a specific mRNA-protein complex formed between the differentiation control element in the 3' untranslated region (UTR) and hnRNPs K and E1. The 3'UTR regulatory complex prevents translation initiation by an unknown mechanism. We demonstrate that the 40S ribosomal subunit can be recruited and scan to the translation initiation codon even when the silencing complex is bound to the 3'UTR. However, the joining of the 60S ribosomal subunit at the AUG codon to form a translation competent 80S ribosome is inhibited, unless initiation is mediated by the IGR-IRES of the cricket paralysis virus. These findings identify the critical step at which LOX mRNA translation is controlled and reveal that 60S subunit joining can be specifically regulated.

3' Untranslated Regions↗
PubMed2001

Genesis of clone size heterogeneity in megakaryocytic and other hemopoietic colonies: the stochastic model revisited.

OBJECTIVE: We previously showed that the distributions of the numbers of doublings (NbD) undergone by individual megakaryocyte progenitors before commitment to polyploidization are markedly skewed and can consistently be fitted to straight lines when plotted on semilogarithmic coordinates. The slope of such lines, which yields the probability of polyploidization per doubling, is made less steep by stimulators of megakaryocyte colony formation and is less steep in mixed erythroid-megakaryocyte than in pure megakaryocyte colonies. Therefore, megakaryocytopoiesis provides a unique model for the study of clonal heterogeneity in a hemopoietic lineage, which is the subject of this review. DATA SOURCES: Articles relevant to the interpretation of these data were selected from the authors' and public databases. DATA SYNTHESIS: Exponential NbD distributions were first explained by postulating that following the assembly of thrombopoiesis-specific regulators, megakaryocyte progenitors require only a single random event to arrest proliferation and commit to polyploidization. However, this stochastic model was refuted by data indicating that intrinsic properties of individual progenitors affect the NbD they achieve. We suggest that the unequal repartition of critical compounds (including receptors, signaling molecules, and gene regulators) inherent in the stem cell-progenitor transition causes a heritable heterogeneity in megakaryocyte progenitor responsiveness to polyploidization inducers. This model would be compatible with 1) the evidence for intraclonal synchronization in megakaryocyte and other hemopoietic clones generated by committed progenitors; 2) the low probability of polyploidization of the relatively insensitive bipotent megakaryocyte progenitors; and 3) the thesis that stimulators act in part by recruiting megakaryocyte progenitor cells endowed with lesser responsiveness to polyploidization inducers and higher proliferative potential. CONCLUSION: The responsiveness of individual megakaryocyte progenitors to polyploidization inducers may be a major determinant of the exponential shape of NbD distributions.

Animals↗
PubMed1999

The erythropoietin receptor.

The erythropoietin (epo) receptor is a member of the cytokine receptor family. It is expressed almost exclusively on erythroid precursor cells and controls the development of red blood cells. The epo receptor has no intrinsic kinase activity, but binds intracellular tyrosine kinases to elicit its signals. Alterations in the transmission of the signalling cascade lead to clinically abnormal red blood cell production.

Animals↗