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PubMed2002

Effects of different us isolates of porcine reproductive and respiratory syndrome virus (PRRSV) on blood and bone marrow parameters of experimentally infected pigs.

Seventy five-week-old, crossbred, caesarean-derived, colostrum-deprived pigs were randomly divided into five groups of 14 pigs and assigned one of five treatments: the intranasal inoculation of 1 (5.7) TCID50 of one of four plaque-purified isolates of porcine reproductive and respiratory syndrome virus (PRRSV) (VR2385, VR2431, ISU-984 and ISU-22), or uninfected cell culture and media. Haematological variables were measured for 21 days and bone marrow was analysed when the pigs were killed three, seven, 10, 21 or 28 days after the inoculation. The PRRSV-infected pigs had non-regenerative anaemia and markedly increased myeloid:erythroid ratios from three to 21 days after inoculation. There was a significant (P < 0.05) difference in the severity of the anaemia induced by the four PRRSV isolates; the most highly pneumovirulent strains (VR2385, ISU-984 and ISU-22) induced more severe anaemia than the least virulent isolate (VR2431). The anaemia induced by PRRSV was probably due to a direct or indirect effect on erythroid precursor cells in the bone marrow.

Anemia↗

PubMed1982

Hemopoietic precursor cells in erythroleukemia.

In order to study the changes in erythroid precursor cells in erythroleukemia, bone marrow cells from 4 patients were cultured for erythroid colony-forming units (CFU-e). The bone marrow from 3 of the patients showed an excess of ringed sideroblasts, and the incidence of CFU-e was very low. The one patient without ringed sideroblasts showed abundant erythroid colony formation. Erythroid colonies of more than eight erythroblasts consisted of normal-appearing erythroblast, while ringed sideroblasts were observed in scattered erythroblasts or in small clusters. The number of granulocyte macrophage colony-forming units (CFU-GM) was markedly lower than normal in all 4 cases. In 2 cases investigated, blast colonies were formed from bone marrow cells under the stimulation of phytohemagglutinin/leukocyte-conditioned medium. These results show that the differentiation of hemopoietic stem cells to erythroid as well as to myeloid cells is affected in erythroleukemia.

Aged↗

PubMed1986

A single amino acid substitution in v-erbB confers a thermolabile phenotype to ts167 avian erythroblastosis virus-transformed erythroid cells.

A library of recombinant bacteriophage was prepared from ts167 avian erythroblastosis virus-transformed erythroid precursor cells (HD6), and integrated proviruses from three distinct genomic loci were isolated. A subclone of one of these proviruses (pAEV1) was shown to confer temperature-sensitive release from transformation of erythroid precursor cells in vitro. The predicted amino acid sequence of the v-erbB polypeptide from the mutant had a single amino acid change when compared with the wild-type parental virus. When the wild-type amino acid was introduced into the temperature-sensitive avian erythroblastosis virus provirus in pAEV1, all erythroid clones produced in vitro were phenotypically wild type. The mutation is a change from a histidine to an aspartic acid in the temperature-sensitive v-erbB polypeptide. It is located in the center of the tyrosine-specific protein kinase domain and corresponds to amino acid position 826 of the human epidermal growth factor receptor sequence.

Alpharetrovirus↗

PubMed1991

Metabolic adaptation during erythropoietin-mediated terminal differentiation of mouse erythroid cells.

Metabolic development was examined in erythroid precursor cells, which were isolated from the spleens of mice infected with the anemia-inducing strain of Friend virus (FVA cells). FVA cells undergo differentiation in vitro from the proerythroblast stage through the reticulocyte stage over a 48-hour period in the presence of erythropoietin. Concomitant with marked decreases in cellular size and energy demand, metabolic capacities of both glycolysis and oxygen consumption diminish after 48 hours in culture by 7- and 18-fold, respectively. Because the oxidative capacity decreases more than glycolytic ability does, the metabolic machinery increasingly shifts toward anaerobic metabolism. During the 48-hour period of differentiation, the 2,3-diphosphoglyceric acid (DPG) content per cell and 2,3-DPG mutase activity per cell increased eightfold and threefold, respectively. Freshly harvested FVA cells have adenosine triphosphate (ATP) levels of 7.23 +/- 2.52 mumol/10(10) cells or 3.76 +/- 1.31 mumol/mL cell water which are 12- or 2.3-fold higher, respectively, than the ATP levels of mature red blood cells. In the course of FVA cell differentiation, ATP content per cell decreases by fourfold, but ATP concentration in cell water remains unchanged because of a corresponding decrease in cellular size and water content during differentiation. These studies show that in the face of dramatic decreases in cell size and cellular energy demand, terminally differentiating erythroid cells maintain a constant ATP level by undergoing an involution of their glycolytic machinery as well as by losing their aerobic metabolic capacity.

2,3-Diphosphoglycerate↗

PubMed1999

Deregulation of erythropoiesis by the Friend spleen focus-forming virus.

The proliferation and differentiation of erythroid cells is a highly regulated process that is controlled primarily at the level of interaction of erythropoietin (Epo) with its specific cell surface receptor (EpoR). However, this process is deregulated in mice infected with the Friend spleen focus-forming virus (SFFV). Unlike normal erythroid cells, erythroid cells from SFFV-infected mice are able to proliferate and differentiate in the absence of Epo, resulting in erythroid hyperplasia and leukemia. Over the past 20 years, studies have been carried out to identify the viral genes responsible for the pathogenicity of SFFV and to understand how expression of these genes leads to the deregulation of erythropoiesis in infected animals. The studies have revealed that SFFV encodes a unique envelope glycoprotein which interacts specifically with the EpoR at the cell surface, resulting in activation of the receptor and subsequent activation of erythroid signal transduction pathways. This leads to the proliferation and differentiation of erythroid precursor cells in the absence of Epo. Although the precise mechanism by which the viral protein activates the EpoR is not yet known, it has been proposed that it causes dimerization of the receptor, resulting in constitutive activation of Epo signal transduction pathways. While interaction of the SFFV envelope glycoprotein with the EpoR leads to Epo-independent erythroid hyperplasia, this is not sufficient to transform these cells. Transformation requires the viral activation of the cellular gene Sfpi-1, whose product is thought to block erythroid cell differentiation. By understanding how SFFV can deregulate erythropoiesis, we may gain insights into the causes and treatment of related diseases in man.

Animals↗

PubMed1984

A and B blood group antigen expression on mixed colony cells and erythroid precursors: relevance for human allogeneic bone marrow transplantation.

Using anti-A and anti-B blood group monoclonal antibodies and fluorescent activated cell sorting of human bone marrow, A (or B) blood group antigen was shown to be on 5.2 +/- 5.9 (mean +/- SD) % of CFU-GEMM and 12.5 +/- 19.6% of the erythroid burst forming cells (designated BFU-GEMM) as defined by the mixed colony assay, and 49.5 +/- 20% of the BFU-E and 83.5 +/- 9.9% of the CFU-E as defined by the erythroid colony assay. This antigen expression on the BFU-GEMM is consistent with the concept that erythroid bursts stimulated by leucocyte conditioned medium are less mature, and are closer in development to the pluripotent stem cell than the BFU-E. These results help to explain the delayed erythropoiesis, and perhaps impaired engraftment of all cell lineages, that may occur in some recipients of ABO incompatible bone marrow transplants with persistent and high anti-A titres.

ABO Blood-Group System↗

PubMed1983

Glycophorin A expression in malignant hematopoiesis.

Two hundred twenty-nine patients with hematopoietic malignancies were tested for reactivity with a monoclonal anti-human glycophorin A antibody. One hundred twenty-three of these cases were classified as acute leukemias of either the myeloid, lymphoid, erythroid, or undifferentiated type. The monoclonal antibody we used (VIE-G4) was obtained after immunization with a human thymocyte suspension. It selectively reacts with glycophorin A (GpA) and strongly binds to 40% of K-562 cells and all morphologically recognizable erythroid precursor cells. Apart from two cases with acute erythroid leukemia, this antibody reacted with none of the malignant cells in the 229 tested hematopoietic malignancies, including the 121 nonerythroid acute leukemias. This finding seems to contradict the earlier observations by L. Andersson and colleagues that a considerable proportion of acute leukemias express GpA on their surface. One reason for this discrepancy might be the fact that VIE-G4 detects only complete glycosylated GpA. If this is the sole explanation, this would mean that the poorly differentiated cells in these cases express incompletely glycosylated GpA.

Acute Disease↗

PubMed1983

Regulation of globin gene expression during induced erythroid cell differentiation.

We can provide increasing insight, albeit still incomplete, into the changes in MELC that accompany induced globin gene expression. It is suggested that these transformed CFU-E-like erythroid precursor cells exhibit in their uninduced state a DNA methylation pattern and globin gene chromatin configuration (DNase I sensitivity) that is compatible with actual or potential gene transcription. Such features may reflect alterations in chromatin configuration that occurred earlier, during the differentiation of erythroid precursor cells, which is associated with the restriction in developmental potential that is characteristic of progression to the CFU-E (or MELC) stage of erythropoiesis. Uninduced MELC display a low level of globin gene transcription, producing globin mRNA or mRNA precursors whose processing or stabilization is the site of action of hemin. The major increase in MELC globin gene transcription that is initiated by HMBA or butyric acid is accompanied by an increase in DNase I hypersensitivity in the regions 5' to the active globin genes. This suggests that reorganization of chromatin structure in the globin gene domains is associated with accelerated globin gene transcription and may be characteristic of a developmental stage transition during terminal differentiation in the erythroid cell lineage.

Animals↗

PubMed1993

A quantitative evaluation of erythropoiesis in myelodysplastic syndromes using multiparameter flow cytometry.

By staining human bone marrow cells with a monoclonal antibody reacting with erythroid precursor cells (AS-E1) and propidium iodide, we have evaluated the proliferative capacity of erythropoiesis in patients with myelodysplastic syndromes (MDS) using flow cytometry. Comparing 36 patients (13 RA/RAS, 13 RAEB, 10 RAEB-t) with 7 normal controls, significant differences in both the percentage of AS-E1+ cells and the fraction of AS-E1+ cells in the S or S-G2M-phase between the four groups were found. Since neither the percentage of AS-E1+ cells nor their fraction in S or S-G2M alone was found to characterize their proliferative activity, we introduced the proliferative fractions of the erythroid cell, i.e. the number of the AS-E1+ cells in S or S-G2M related to all bone marrow cells in S or S-G2M. Applying these parameters, we found significantly increased proliferative AS-E1 fractions in the RA/RAS group compared to the normal controls (p = 0.03 and 0.002) respectively, as well as a highly significant decrease with disease progression.

Antibodies, Monoclonal↗

PubMed1989

Parvovirus infection in children.

Human parvovirus, discovered fortuitously in 1975, is probably most often associated with an asymptomatic or mild nonspecific illness. This small DNA virus, like other members of the Parvoviridae, has a predeliction for rapidly growing cells, especially the erythroid precursor cells of bone marrow. The virus has now clearly been associated with specific clinical syndromes. Epidemiologic and experimental evidence clearly document human parvovirus as the etiologic agent of the acute aplastic crisis associated with various forms of chronic hemolytic anemia. It is also the etiologic agent of erythema infectiosum, the most frequent presentation of acute parvovirus infection in the normal child. The rash of erythema infectiosum is faint and evanescent and may not always be present or recognized, especially in black children. Frequently this infection may occur as a nonspecific viral syndrome in children or adults, accounting for the high incidence of seropositivity among adults despite an infrequent history of erythema infectiosum. The attack rate is highest among 7- to 10-year old contacts. Severe infection in the fetus has been associated with second trimester abortion. Persistent infection in an immunocompromised child has been associated with chronic aplasia of all marrow elements, suggesting the importance of a normal host immune system to contain this infection. The arthritis and arthralgia seen in older patients, especially women, occur after the viremia has ended, suggesting a possible immunologic pathogenesis for this complication. Volunteer studies have delineated the time course of the various manifestations of parvovirus infection. The ability to infect volunteers intranasally and the finding of virus in respiratory secretions suggests that this may be the route of spread to susceptible contacts.

Child↗

PubMed1983

Induction of globin gene expression during erythroid cell differentiation.

We can provide increasing insight, albeit still incomplete, into the changes in MELC that accompany globin gene expression induced by polar chemicals, such as DMSO, and other agents. These transformed, CFUe-like erythroid precursor cells exhibit in their uninduced state, a DNA methylation pattern and globin gene (formula; see text) chromatin configuration (DNase I sensitivity) that is compatible with actual or potential gene transcription. Such features may reflect alterations in chromatin configuration that have occurred at a stage prior to leukemic transformation, during the differentiation of earlier erythroid precursor cells and associated with the restriction in developmental potential characteristic of progression to the CFUe (or MELC) stage of erythropoiesis. Uninduced MELC display a low level of globin gene transcription, producing globin mRNA or mRNA precursors whose processing or stabilization is the target of action of hemin. The major increase in MELC globin gene transcription that is initiated by DMSO, HMBA, or butyric acid, is accompanied by, and perhaps preceded by, an increase in DNase I hypersensitivity in the regions 5' to the active globin genes. This suggests that reorganization of chromatin structure in the globin gene domains is associated with accelerated globin gene transcription and may be characteristic of a developmental transition during terminal differentiation in the erythroid cell lineage.

Animals↗

PubMed1978

Sequential methylation of globin mRNA in nucleated erythroid cells and reticulocytes of mice.

The order of methylation of the 5'-terminus of globin mRNA of mice was studied by incubation of staged nucleated erythroid cells and peripheral reticulocytes with [methyl-3H] methionine. Methylation of the 5'-termini of alpha and beta- globin mRNAs in enucleated reticulocytes was demonstrated as follows: (a) [methyl-3H] incorporation into poly(A)+ RNA of reticulocytes co-migrated with the alpha- and beta- globin mRNAs on gel electrophoresis, and (b) following digestion of this RNA, radioactivity was localized to the four methyl sites at the 5'-capped structure of mouse globin mRNAs. However, this methylation is only 5 to 8% as efficient as in nucleated erythroid precursor cells, suggesting that most globin mRNA molecules are fully methylated prior to the reticulocyte stage. Incubations of early and late nucleated erythroid precursor cells and pulse-chase experiments with reticulocytes demonstrate that addition of the four 5'-terminal methyl groups follows an orderly sequence. In addition, the pulse-chase experiments suggest the turnover of the N7-methyl group on the 5'-terminal guanosine, but not of the other methyl groups in the 5'-terminus of globin mRNA. Thus, 5'-terminal methylation of globin mRNA is a nonrandom, dynamic process.

Animals↗

PubMed1977

Biochemical characterization of RNA and protein synthesis in erythrocyte development.

Newts (Triturus cristatus) made anemic with acetylphenylhydrazine (APH) fail to regenerate erythrocytes (RBC's) immediately and exhibit a latent period of 1.5-2 wk during which animals lack RBC's and are aplastic. With the establishment of erythroid regeneration at 10-14 days, relatively homogeneous populations of successive erythropoietic stages occur in the blood. This feature makes possible biochemical analyses of events in early, intermediate, and late developmental stages, respectively, each of which can be obtained in vivo with minimal contamination by other stages. Previous studies have described a primitive cell population referred to as "erythroid precursor cells" (EPC's) which precedes the appearance of definitive erythroid elements. The present studies show that EPC's and early erythroid cells are engaged mainly in ribosomal production, including synthesis of rRNA and ribosomal proteins. Moreover, EPC's and early erythroid cells also synthesize tRNA and a presumed Hb-mRNA which has been identified by its sedimentation rate at 9-12 s and its content of polyadenylic acid. In intermediate stages, there occurs a fourfold decrease in the level of RNA synthesis and, while rRNA continues to be formed, there is a disproportionate accumulation of the two major cytoplasmic rRNA species in favor of the large ribosomal subunit RNA. In late developmental stages, the level of RNA synthesis is markedly diminished with little or no evidence of formation of defined RNA classes. Correlated radioautographic and biochemical studies with radioactive delta-aminolevulinic acid and leucine indicate that EPC's and other early erythroid elements synthesize not only hemoglobin but also ferritin and ribosomal proteins. It is concluded that: (a) erythroid RNA synthesis is most pronounced in the early developmental stages, being manifested predominantly by rRNA production but including tRNA and Hb-mRNA; (b) intermediate developmental stages show both "ribosomal wastage" and decreased growth rate, marking a pivotal point between the transcriptional activities of early stages and translational activities of late stages; (c) EPC's represent a cell population already committed to RBC formation and are excluded from a role as the pluripotential stem cell.

Animals↗

PubMed1992

Developmental changes in erythropoietin receptor expression of fetal mouse liver.

Erythropoietin (EPO) stimulates proliferation and differentiation of late erythroid precursor cells (CFU-E) and thereby determines the rate of erythropoiesis. Liver is the major erythropoietic site in a fetus. We dealt with developmental changes in CFU-E and EPO receptor (EPO-R) of fetal mouse liver. The affinity of the EPO-R to EPO was unchanged during fetal development. The population size of CFU-E, the number of EPO-R per liver cell, and EPO-R mRNA decreased as gestation proceeded, in a pattern indicating that the expression of EPO-R on erythroid precursor cells in fetal mouse liver is governed mostly by the process of mRNA production.

Animals↗

PubMed1982

Synthesis and maturation of the erythrocyte anion transport protein--an internal sequence for membrane insertion.

The biosynthesis of the erythrocyte anion transport glycoprotein, Band III (Mr 100,000), is of interest, as its N-terminal half is hydrophilic and faces the cytoplasmic surface; the C-terminal half spans the phospholipid bilayer several times. Band III is synthesized by erythroid precursor cells obtained from the spleens of anaemic mice. Newly synthesized Band III was inserted into rough endoplasmic reticulum membranes with an asymmetric orientation which resembled that of mature Band III in erythrocyte membranes: the N-terminal portion of the molecule facing the cytoplasm. Newly made Band III contained a high-mannose asparagine-linked oligosaccharide, which was susceptible to cleavage by endoglycosidase H. During the next 20-30 min, this oligosaccharide was processed to a form resistant to endoglycosidase H degradation, presumably in the Golgi complex. The processed Band III was subsequently expressed on the cell surface, at about 30-45 min after synthesis. To study the mechanism of insertion of Band III into microsomes, we used erythroid precursor cells from the spleens of anaemic mice as a source of messenger RNA for studies in vitro 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 microsomal membranes in its mature configuration, with the N-terminal portion exposed to the cytoplasm and its hydrophobic C-terminal portion spanning the lipid bilayer. The newly-synthesized Band III was also provided with a high-mannose asparagine-linked oligosaccharide. Band III was found to be inserted into dog pancreatic microsomes in a co-translational manner; in synchronized translation studies microsomes could be added as late as the time when the hydrophilic N-terminal half of the protein had been synthesized and still allow normal trans-membrane insertion and glycosylation. There is no cleavage of any N-terminal peptide during membrane insertion. In many respects, therefore, the biosynthesis of Band III resembles that of co-translationally-inserted proteins whose N-terminal portions are exposed on the exterior of the cell, like vesicular stomatitis virus glycoprotein, HLA-A antigens, and glycophorin. However, our results suggest that Band III contains a sequence near the middle of the protein which directs its insertion into endoplasmic reticulum membranes.

Acetylglucosaminidase↗

PubMed1992

Enhanced expression of interleukin-3 and granulocyte-macrophage colony-stimulating factor receptor subunits in murine hematopoietic cells stimulated with hematopoietic growth factors.

AIC2A and AIC2B are closely related genes encoding components of the receptors for murine interleukin-3 (IL-3) (AIC2A) and granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-5 (AIC2B). We have studied the parallel regulation of expression of these genes in erythroid and myeloid progenitor cell lines. AIC2A and AIC2B transcription was transiently induced in these cells in response to a variety of hematopoietic growth factors, including erythropoietin (EPO), monocyte-CSF, IL-3, GM-CSF, and stem cell factor (SCF or kit ligand). Run-on assays established that the increase occurred mainly at the transcriptional level. Immunoprecipitation experiments confirmed that the increase in messenger RNA expression resulted in augmented synthesis of both AIC2A and AIC2B proteins, and binding studies further showed these proteins to be functional. We observed a fourfold increase in low-affinity IL-3 sites in an erythroid precursor cell line stimulated with EPO, and a threefold increase in GM-CSF high-affinity sites in a myeloid cell line stimulated with IL-3. In addition, we showed that the increase in the IL-3 receptor chain AIC2A in the erythroid precursor cell line correlated with the ability of IL-3 to exert a cooperative effect with EPO in the induction of beta-globin in these cells.

Base Sequence↗

PubMed1981

The use of ferrokinetics in the study of experimental anemia.

Erythropoietic cells in bone marrow are vulnerable to cytotoxic substances. There are three types of erythroid precursors: cells that can take up Fe but do not proliferate (reticulocytes), those that can take up Fe and proliferate (normoblasts and pronormoblasts), and those cells that do not take up Fe but can proliferate and differentiate into the erythroid cell line (ERC and stem cells). Each of these erythroid precursors requires a certain time before they emerge into the peripheral blood as mature red blood cells. By applying our understanding of ferrokinetics associated with erythropoiesis, it was possible to estimate a cytotoxic effect of chemicals on proliferating erythgroid precursors (pronormoblasts) in mice by measuring 24-hr 59Fe uptake in red blood cells 48 hr after treatment with chemicals. The effect of chemicals on pluripotent hemopoietic stem cells in mice was also estimated by measuring 24-hr 59Fe uptake 72 hr after treatment with chemicals. The validity of experimental schemes was tested using cytarabine, methotrexate, vinblastine, cyclophosphamide, and busulfan, which are known to act against specific cell types. Effects on pluripotent hemopoietic stem cells were tested with or without activation of stem cells in G0 into cell cycle. Applications of the 59Fe uptake method in the study of (1) benzene toxicity and (2) effect of pentobarbital on the toxic action of hydroxyurea and cytarabine are described. Proper application of the ferrokinetic characteristics of erythropoietic cells enables the establishment of a methodology which can be used to evaluate potential toxic effects of chemicals on erythroid precursor cells and pluripotent hemopoietic stem cells.

Anemia↗

PubMed2006

Chronic polyarthritis caused by mammalian DNA that escapes from degradation in macrophages.

A large amount of chromosomal DNA is degraded during programmed cell death and definitive erythropoiesis. DNase II is an enzyme that digests the chromosomal DNA of apoptotic cells and nuclei expelled from erythroid precursor cells after macrophages have engulfed them. Here we show that DNase II-/-IFN-IR-/- mice and mice with an induced deletion of the DNase II gene develop a chronic polyarthritis resembling human rheumatoid arthritis. A set of cytokine genes was strongly activated in the affected joints of these mice, and their serum contained high levels of anti-cyclic citrullinated peptide antibody, rheumatoid factor and matrix metalloproteinase-3. Early in the pathogenesis, expression of the gene encoding tumour necrosis factor (TNF)-alpha was upregulated in the bone marrow, and administration of anti-TNF-alpha antibody prevented the development of arthritis. These results indicate that if macrophages cannot degrade mammalian DNA from erythroid precursors and apoptotic cells, they produce TNF-alpha, which activates synovial cells to produce various cytokines, leading to the development of chronic polyarthritis.

Animals↗