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PubMed1998

Vascularization in the murine allantois occurs by vasculogenesis without accompanying erythropoiesis.

The aim of this study was to determine whether the blood vessels of the murine allantois are formed by vasculogenesis or angiogenesis. Morphological analysis revealed that differentiation of allantoic mesoderm into an outer layer of mesothelium and an inner vascular network begins in the distal region of the allantois, which is most remote from other tissues, as early as the late neural plate stage (approximately 7.75 days postcoitum). Nascent blood vessels were not found in the base of the allantois until 4-somite pairs had formed in the fetus (approximately 8.25 days postcoitum), and vascular continuity with the yolk sac and fetus was not present until the 6-somite-pair stage (approximately 8.5 days postcoitum). Immunohistochemical analysis demonstrated that flk-1, a molecular marker of early endothelial cells, is expressed in significantly more distal than basal core cells in the early allantois and never in mesothelium. Furthermore, synchronous grafting of donor yolk sac containing blood islands into blood islands of headfold-stage host conceptuses provided no evidence that the yolk sac contributes endothelial cells to the allantois. Finally, when removed from conceptuses and cultured in isolation, neural plate and headfold-stage allantoises formed a conspicuous vascular network that was positive for Flk-1. Hence, the vasculature of the allantois is formed intrinsically by vasculogenesis rather than extrinsically via angiogenesis from the adjacent yolk sac or fetus. Whether allantoic vasculogenesis is associated with erythropoiesis was also investigated. Benzidine-staining in situ revealed that primitive erythroid cells were not identified in the allantois until 6-somite pairs when continuity between its vasculature and that of the yolk sac was first evident. Nevertheless, a small number of allantoises removed from conceptuses at a considerably earlier stage were found to contain erythroid precursor cells following culture in isolation. To determine whether such erythroid cells could be of allantoic origin, host allantoises were made chimeric with lacZ-expressing donor allantoises that were additionally labeled with [3H]methyl thymidine. Following culture and autoradiography, many lacZ-expressing benzidine-stained cells were observed in donor allantoises, but none contained silver grains above background. Moreover, no cells of donor allantoic origin were found in the fetus or yolk sac. Hence, vasculogenesis seems to be independent of erythropoiesis in the allantois and to involve a distal-to-proximal gradient in differentiation of allantoic mesoderm into the endothelial cell lineage. Furthermore, this gradient is established earlier than reported previously, being present at the neural plate stage.

Allantois↗
PubMed1995

Enhancement of erythroid colony growth by triiodothyronine in cell cultures from bone marrow of normal and anemic rats with chronic renal failure.

In order to make a contribution in clarifying the role of thyroid hormones on modulation of erythropoiesis and to gain a further insight on the effects of these hormones in the anemia of chronic renal failure (CRF), we studied the action of triiodo-1-thyronine (LT3) and DT3, a dextrorotary non-calorigenic isomer of T3 on late (CFU-E) and early (BFU-E) committed erythroid precursor cells from bone marrow of normal and anemic uremic rats. Cultures were prepared using the methylcellulose technique containing a standard dose (182 mU/ml) of erythropoietin (Ep), LT3 and DT3 in doses of 0.5 and 1.5 micrograms/ml. Thyroid hormones were added to cultures in the absence of Ep. Our results demonstrated that LT3 and DT3 produced a direct and significant stimulation of CFU-E formation and a moderate increase of BFU-E. A dose-correlation was apparent in cultures containing thyroid hormones. DT3 was somewhat less active than LT3. As expected, Ep also produced a significant increase in erythroid colony formation, mainly CFU-E. It is notheworthy that the effects of LT3, DT3 and Ep on erythroid colony growth were significantly higher in marrow cultures from anemic rats with CRF, indicating an increased proliferative cell kinetics of committed erythroid cells in response to these drugs.

Anemia↗
PubMed1996

Silencing of human fetal globin expression is impaired in the absence of the adult beta-globin gene activator protein EKLF.

Globin genes are subject to tissue-specific and developmental stage-specific regulation. A switch from human fetal (gamma)-to adult (beta)-globin expression occurs within erythroid precursor cells of the adult lineage. Previously we and others showed by targeted gene disruption that the zinc finger gene, erythroid Krüppel-like factor (EKLF), is required for expression of the beta-globin gene in mice, presumably through interaction with a high-affinity binding site in the proximal promoter. To examine the role of EKLF in the developmental regulation of the human gamma-globin gene we interbred EKLF heterozygotes (+/-) with mice harboring a human beta-globin yeast artificial chromosome transgene. We find that in the absence of EKLF, while human beta-globin expression is dramatically reduced, gamma-globin transcripts are elevated approximately 5-fold. Impaired silencing of gamma-globin expression identifies EKLF as the first transcription factor participating quantitatively in the gamma-globin to beta-globin switch. Our findings are compatible with a competitive model of switching in which EKLF mediates an adult stage-specific interaction between the beta-globin gene promoter and the locus control region that excludes the gamma-globin gene.

Adult↗
PubMed1998

Knock-in mutation of transcription factor GATA-3 into the GATA-1 locus: partial rescue of GATA-1 loss of function in erythroid cells.

Transcription factors of the GATA-family are essential for proper development of diverse tissues or cell types. GATA-1 is required for differentiation of two hematopoietic lineages (red blood cells and megakaryocytes), whereas GATA-3 is essential for T-cell development. Functional studies suggest that many properties of the GATA-family of proteins are shared and largely interchangeable. To test whether the function of GATA-1 in erythroid differentiation can be replaced by another GATA-factor, we generated a knock-in mutation of the GATA-1 locus in which GATA-3 cDNA was introduced by gene targeting. Mutant embryos (designated G1G3ki), though embryonic lethal, exhibit partial rescue, characterized by increased survival of erythroid precursor cells and improved hemoglobin production. The basis for the incomplete extent of rescue is likely to be complex, but may be accounted for, in part, by insufficient accumulation of GATA-3 protein (compared with the normal level of GATA-1). Our findings suggest that GATA-3 protein is functional when expressed in an erythroid environment and is competent to act on at least a subset of erythroid-expressed target genes in vivo.

Anemia↗
PubMed1991

The importance of N- and O-linked oligosaccharides for the biosynthesis and in vitro and in vivo biologic activities of erythropoietin.

Erythropoietin (EPO) plays a critical role in stimulating the proliferation and differentiation of erythroid precursor cells. EPO is heavily glycosylated with three asparagine (N)-linked tetraantennary oligosaccharides that may contain N-acetyl-lactosamine repeats and a single serine (O)-linked oligosaccharide. EPO expressed in Chinese hamster ovary cells exhibits biologic properties and amino acid and carbohydrate composition similar to natural urinary EPO. The importance of the complex N-linked and the O-linked carbohydrate was studied by expressing EPO in cells that are deficient in UDP-galactose/UDP-N-acetylgalactosamine 4-epimerase activity. In these cells, the ability to add galactose and N-acetylgalactosamine to glycoproteins can be controlled by the addition of these sugars to the culture medium. The results demonstrate that a block in O-linked glycosylation and/or the ability to process N-linked carbohydrate to completion does not alter EPO secretion. EPO produced without O-linked carbohydrate exhibits normal in vitro and in vivo biologic activity and in vivo clearance. However, EPO produced with incompletely processed N-linked oligosaccharides exhibits normal in vitro activity but is at least 500-fold less effective in stimulating erythropoiesis in vivo. Studies on the survival of bioactive EPO remaining in the circulation demonstrated that EPO with incomplete N-linked oligosaccharides exhibits a sevenfold increased rate of clearance. However, this increased clearance may not fully account for the 500-fold loss of in vivo activity. These results suggest a potentially important unique requirement for appropriate complex N-linked oligosaccharides for the intrinsic biologic activity of EPO in vivo.

Acetylgalactosamine↗
PubMed1999

A case of cutaneous extramedullary hematopoiesis in myelofibrosis with a preponderance of eosinophilic precursor cells.

A 48-year-old Korean man with myelofibrosis had erythematous papules and nodules on his scalp, anterior chest, back, lower abdomen, and both thighs. Skin biopsy showed cellular infiltration on the perivascular dermis and subcutaneous fat. Infiltrates were composed mainly of myeloid cells, especially of eosinophilic precursor cells. Erythroid and a few megakaryocytic precursors were also found. We diagnosed cutaneous extramedullary hematopoiesis with an interesting preponderance of eosinophilic precursor cells.

Biopsy, Needle↗
PubMed2006

Polyamines as an inhibitor on erythropoiesis of hemodialysis patients by in vitro bioassay using the fetal mouse liver assay.

The pathogenesis of anemia in patients with chronic renal failure has been greatly attributed to erythropoietin (EPO) deficiency. Recently, however, there has been some thought that uremic inhibitors might suppress the activity of EPO and reduce the maturation of erythropoiesis. Polyamines are well known to be involved in the regulation of cellular proliferation and differentiation. Furthermore, the polyamine levels in the serum or erythrocytes are elevated in chronic hemodialysis patients, and can be lowered immediately by hemodialysis. In the present study, we first measured the polyamines levels (putrescine, spermidine, spermine) by high performance liquid chromatography (HPLC) in 20 chronic hemodialysis patients, and investigated the effects of polyamines on erythropoiesis by in vitro bioassay using fetal mouse liver cells. The direct effects of polyamines in erythroid colony formation in the medium with and without EPO were evaluated. Each polyamine level in chronic hemodialysis patients was higher than in the healthy subjects, and a significant negative correlation was found between polyamines and erythropoiesis. Polyamines inhibited the activity of EPO, but they did not have any direct effect on colony formation of the fetal mouse liver cells. These results suggest that polyamines have inhibitory effects on the proliferation or maturation of erythroid precursor cells and are intimately involved in the pathogenesis of renal anemia in chronic hemodialysis patients.

Adolescent↗
PubMed2000

Ferritin expression in maturing normal human erythroid precursors.

We studied the expression of H- and L-ferritin subunits at sequential stages of maturation of normal human erythroid precursors. The erythroid cells developed in liquid culture and were purified immunomagnetically before analysis. It was found that the content of both ferritin subunits decreased exponentially with maturation: the decrease was rapid when cellular haemoglobin was low, and it slowed down when the haemoglobin was increased. This mode of decline was especially pronounced for the L-subunits. The H-/L-subunit ratio did not change significantly during the investigated period. The synthesis of both subunits was equal at each given developmental stage, and declined significantly with maturation. However, this decline was just slightly faster than that of total protein synthesis. The data indicated that the degradation of H- and L-ferritin also declined as maturation proceeded. No decrease was observed in mRNA levels of either ferritin subunit. Thus, the ferritin content and turnover were maximal at the beginning of haemoglobin accumulation and diminished later. As the rate of ferritin turnover determines the rate of incorporation and release of its iron, the results presented suggest that ferritin mediates cellular iron transport and donates iron for haem synthesis, mainly at the beginning of haemoglobin accumulation. The synthesis of both ferritin subunits is regulated during erythroid maturation at the post-transcriptional level.

Cell Division↗
PubMed1982

Canine cyclic haematopoiesis: the effect of endotoxin on erythropoiesis.

We have examined the effects of chronic endotoxin treatment on erythropoiesis in six grey collies with cyclic haematopoiesis. Blood reticulocytes, bone marrow erythroid colony (EC) forming cells, serum iron and erythropoietin (ESF) values showed regular periodic fluctuations in untreated grey collies. Daily endotoxin injections eliminated the cyclic fluctuations of reticulocytes and EC. The mean serum iron values were increased and recurrent hypoferraemia eliminated, while the mean serum ESF values were reduced. The cyclic fluctuations of serum ESF values were no longer apparent in the endotoxin treated grey collies. Tritiated thymidine suicide of the marrow EC forming cells failed to show cyclic changes either in untreated or endotoxin treated dogs. The ESF sensitivity of EC in the grey collie was unchanged during endotoxin treatment and was not different from normal dogs. Endotoxin appears to alter periodic erythropoiesis by stabilizing the flux of cells into the committed erythroid precursor cell pool from a more primitive stem cell compartment.

Animals↗
PubMed2003

Preinfection treatment of resistant mice with CpG oligodeoxynucleotides renders them susceptible to friend retrovirus-induced leukemia.

We recently reported that immunostimulatory oligodeoxynucleotides (CpG oligodeoxynucleotides [CpG-ODN]) were effective in postexposure treatment of retrovirus-induced disease (A. R. M. Olbrich et al., J. Virol. 76:11397-11404, 2002). We now show that the timing of treatment is a critical factor in treatment efficacy. In stark contrast to the success of postexposure treatments, we found that CpG treatment of susceptible mice prior to Friend retrovirus infection accelerated the development of virus-induced erythroleukemia. Furthermore, 70.8% of mice that were resistant to Friend virus-induced leukemia developed disease after inoculation of CpG-ODN before infection. The CpG pretreatment of these mice enhanced viral loads in their spleens and blood compared to controls that received ODN without CpG motifs. The main target cells of Friend virus, erythroid precursor cells and B cells, proliferated after CpG-ODN inoculation and provided an enlarged target cell population for viral infection. Our present findings together with our previous report demonstrate that CpG-ODN treatment of viral infections may be a double-edged sword that can result in an effective therapy but also in an acceleration of disease progression depending on the time point of treatment.

Adjuvants, Immunologic↗
PubMed1977

Studies on erythroid-committed precursor cells in the polycythaemic mouse.

The erythropoietin responsiveness of mice maintained in a polycythaemic condition for 42 days by transfusion of syngeneic red blood cells (but otherwise untreated) remained unchanged throughout the whole of that time. Furthermore the cycling rate, as measured by 3H-thymidine killing, also remained unchanged. These results indicate that continuous production and amplification of erythropoietin-responsive cells continues for long periods in the absence of demand for mature erythrocytes. It has also been shown that the erythropoietin response in the experimentally-induced polycythaemic mouse can be transiently increased as a result of "priming" injections of EPO. This suggests that the size of the erythropoietin-responsive cell (ERC) population has been increased, presumably by inducing extra division in the pre-ERC during maturation. This has previously been shown to occur only under conditions of drug induced depletion of both CFU-S and of ERC.

Animals↗
PubMed2003

Human parvovirus B19 nonstructural protein (NS1) induces cell cycle arrest at G(1) phase.

Human parvovirus B19 infects predominantly erythroid precursor cells, leading to inhibition of erythropoiesis. This erythroid cell damage is mediated by the viral nonstructural protein 1 (NS1) through an apoptotic mechanism. We previously demonstrated that B19 virus infection induces G(2) arrest in erythroid UT7/Epo-S1 cells; however, the role of NS1 in regulating cell cycle arrest is unknown. In this report, by using paclitaxel, a mitotic inhibitor, we show that B19 virus infection induces not only G(2) arrest but also G(1) arrest. Interestingly, UV-irradiated B19 virus, which has inactivated the expression of NS1, still harbors the ability to induce G(2) arrest but not G(1) arrest. Furthermore, treatment with caffeine, a G(2) checkpoint inhibitor, abrogated the B19 virus-induced G(2) arrest despite expression of NS1. These results suggest that the B19 virus-induced G(2) arrest is not mediated by NS1 expression. We also found that NS1-transfected UT7/Epo-S1 and 293T cells induced cell cycle arrest at the G(1) phase. These results indicate that NS1 expression plays a critical role in G(1) arrest induced by B19 virus. Furthermore, NS1 expression significantly increased p21/WAF1 expression, a cyclin-dependent kinase inhibitor that induces G(1) arrest. Thus, G(1) arrest mediated by NS1 may be a prerequisite for the apoptotic damage of erythroid progenitor cells upon B19 virus infection.

Cell Cycle↗
PubMed1983

Rabbit red blood cell hexokinase. Mechanism of decay during cell life-span.

Rabbit red blood cells contain hexokinase type I whereas in the reticulocyte two distinct molecular forms (HK Ia and Ib) are present. One (HK Ia) corresponds to hexokinase type I from other tissues, while the other differs from any previously reported isozyme. Rabbit bone marrow cells contain hexokinase type I and II. However, when the erythroid precursor cells become predominant over the non-erythroid cells (during phenylhydrazine anemia) a great increase of HK Ia can be observed concomitant with the appearance of HK Ib. Fractionation of the bone marrow cells on density gradients provides evidence that basophil erythroblasts and proerythroblasts contain only HK Ia while HK Ib appears at the reticulocyte stage. Maturation and ageing of circulating reticulocytes are associated with the decrease of hexokinase activity. Since the decay rate of HK Ib is about three times higher than the decay rate of HK Ia, the mature erythrocytes do not contain appreciable amounts of HK Ib. Furthermore, in vitro, HK Ia and Ib possess similar stabilities so that a cellular mechanism must be responsible of their in vivo different decay rates. This mechanism, as reported in this paper, is ATP-dependent, could be found in the soluble fraction, and is active only at the reticulocyte stage. These properties are similar to those of the ATP-dependent proteolytic system. Pure ubiquitin, an essential polypeptide of the ATP-dependent proteolytic system, is also able to catalyze the decay of hexokinase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Transient myeloproliferative disorder with erythroid differentiation in Down syndrome.

A newborn with a karyotype of 47, XY, +21 presented at birth with a white blood cell count of 27 700/microL of which 61% were blast cells. The blast cell morphologic structure was initially not characteristic of any particular lineage, although the cytoplasm contained fine granules and occasional small vacuoles. Routine cytochemical stains were negative, except one for nonspecific esterase that was faintly positive in most of the blast cells. Flow cytometric analyses showed that the blast cells expressed glycophorin A with a subset dimly coexpressing CD45 and were negative for CD34, CD71, myeloid, lymphoid, and platelet-associated antigens. These immunophenotypic findings were consistent with an abnormal erythroid phenotype. A few days postpartum, markedly dysplastic erythroid precursor cells appeared in the peripheral blood and increased in number as the early blast cells decreased. After a period of subdued blast cell production, a second wave of increase in the number of blast cells and dysplastic erythroblasts followed and ended with the disappearance of circulating abnormal cells. The child is now 5 years old and no major illness has been reported since the remission of this disorder. This case most likely belongs to the category of transient myeloproliferative disorders, although the erythroid-like phenotype of blast cells and the evidence of single-lineage maturation to circulating dysplastic erythroid precursors allow the suggestion that this process could represent a special form of a self-limited hematologic disorder in Down syndrome.

Cell Differentiation↗
PubMed2005

Differential amplification of murine bipotent megakaryocytic/erythroid progenitor and precursor cells during recovery from acute and chronic erythroid stress.

Two murine bipotent erythroid/megakaryocytic cells, the progenitor (MEP) and precursor (PEM) cells, recently have been identified on the basis of the phenotypes of linnegc-kitposSca-1neg CD16/CD32lowCD34low and TER119pos4A5pos or 2D5pos, respectively. However, the functional relationship between these two subpopulations and their placement in the hemopoietic hierarchy is incompletely understood. We compared the biological properties of these subpopulations in marrow and spleen of mice with and without acute or chronic erythroid stress. MEP cells, but not PEM cells, express c-kit, respond to stem cell factor in vitro, and form spleen colonies in vivo. PEM cells comprise up to 50%-70% of the cells in BFU-E-derived colonies but are not present among the progeny of purified MEP cells cultured under erythroid and megakaryocytic permissive conditions. PEM cells increase 10- to 20-fold under acute and chronic stress, whereas MEP cell increases (21%-84%) are observed only in acutely stressed animals. These data suggest that MEP and PEM cells represent distinct cell populations that may exist in an upstream-downstream differentiation relationship under conditions of stress. Whereas the dynamics of both populations are altered by stress induction, the differential response to acute and chronic stress suggests different regulatory mechanisms. A model describing the relationship between MEP, PEM, and common myeloid progenitor cells is presented.

Animals↗
PubMed1995

Negative regulation of chicken GATA-1 promoter activity mediated by a hormone response element.

GATA-1 is a DNA-binding protein that regulates transcription of erythroid-specific genes and is required for the formation of mature erythroid cells. We show here that the GATA-1 hormone response-like element (GHRE) within the first intron of the gene functions as an inhibitory element in chicken erythroid precursor cells, as revealed by expression studies with mutants of the minimal GATA-1 promoter. We identify in these precursor cells the relevant proteins that interact with GHRE as a heterodimer of the thyroid hormone receptor alpha and the chicken ovalbumin upstream promoter transcription factor. Our results indicate that this novel complex can negatively regulate the GATA-1 promoter and suggest that GATA-1 can overcome this inhibitory action. We provide evidence that the viral gene product, v-erb A, can also reduce GATA-1 promoter activity through the GHRE site.

Animals↗
PubMed2004

Tetrodotoxin-sensitive Na+ channels and muscarinic and purinergic receptors identified in human erythroid progenitor cells and red blood cell ghosts.

This article concerns the identification of different types of voltage-gated Na(+) channels and of muscarinic and purinergic receptors that are expressed in human erythroid precursor cells and red cell ghosts. We analyzed, by RT-PCR, RNA that was extracted from purified and synchronously growing human erythroid progenitor cells, differentiating from erythroblasts to reticulocytes in 7 to 14 days. These extracts were free of white cell and platelet contamination. Two types of voltage-gated, tetrodotoxin-sensitive Na(+) channels were found. These were Na(v)1.4 and Na(v)1.7, the former known to be present in skeletal muscle and the latter in peripheral nerve. By using a pan Na(+) channel antibody and Western blotting, an immunoreactive channel was detected in ghosts of human red blood cells, consistent with the expression of these two channels. The transcripts for four of the five known subtypes of muscarinic receptors were also identified, including subtypes M2, M3, M4, and M5, whereas subtype M1 was not found. Expression was also detected for the purinergic type receptors P2X(1), P2X(4), P2X(7), and P2Y(1) whereas types P2Y(2), P2Y(4), and P2Y(6) were not found. We also searched for but did not find transcripts for hBNP-1, a type 1b human brain sodium phosphate cotransporter, and cystic fibrosis transmembrane conductance regulator (CFTR). Implications regarding the presence of these different types of channels and receptors in human red blood cells and their functional significance are discussed.

Base Sequence↗