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PubMed1975

Erythropoietin responsiveness in polycythaemia vera.

A liquid bone marrow culture technique was used to study erythropoiesis in polycythaemia vera. Three patients with the diagnosis of polycythaemia vera treated only by phlebotomy were compared to three healthy volunteers. Erythropoiesis in vitro was assessed by counts of nucleated red cells and 3H-thymidine incorporation into erythroid precursors. Human urinary erythropoietin was found to stimulate erythropoiesis in cultures from the polycythaemia patients as well as normals. The erythropoietin effect was blocked by a rabbit anti-erythropoietin antibody. These results suggest that some erythroid precursor cells maintain an intact erythropoietin response mechanism in polycythaemia vera. They also support clinical studies of this disorder indicating that some regulation by erythropoietin may occur in vivo.

Cell Count↗

PubMed1975

[Normal erythropoiesis].

The organism has at least three different mechanisms for the modulation of oxygen supply to tissues: 1) respiratory-circulatory, 2) modification of oxygen dissociation of hemoglobin, 3) modification of oxygen transport capacity by increasing the volume of circulating red cells. The erythroid, granulocytic and thrombocytic cell lines originate from a common pluripotent stem cell. In the course of differentiation the erythroid precursor cell acquires the capability of responding to the humoral regulator of total red blood cell volume, erythropoietin. Furthermore, the ability develops to take up tightly bound iron from transferrin, to synthesize large amounts of hemin and to express the few structural genes for hemoglobin polypeptides preferentially. The effects of these phenomena are discussed in the framework of the erythron.

Biological Transport↗

PubMed1979

Fetal hemoglobin in polycythemia vera: cellular distribution in 50 unselected patients.

Fetal hemoglobin was studied in 50 unselected patients with polycythemia vera with chemical determinations of Hb F and measurements of F-cell levels using fluorescent anti-Hb F antibodies. Although in the majority of the patients Hb F production did not differ from that in normal controls, in 20% of the patients F-cell values were above the normal range. There was no correlation between F-cell values and duration of disease, treatment modality, presence of myelofibrosis, or hematologic parameters at the time of study. In 5 of 50 patients 30%--45% of the erythrocytes contained Hb F; such striking elevations of F cells may reflect a distorted differentiation of erythroid precursor cells in certain patients with this disorder.

Erythrocytes↗

PubMed1979

Characterization of a Friend virus-replicating target cell.

The FV-replicating target cell characterized in this study is an erythroid precursor cell, as shown by its response to bleeding and hypertransfusion. The target cell is not identical with the BFU-E compartment as demonstrated by different model velocities and different cell cycle characteristics as compared to BFU-E. Different sensitivity of FV-target cells and CFU-E to AMD, differences in the growth kinetics of both cell populations in bone marrow and spleen of mice after bleeding, and large quantitative differences of both cell populations in hemopoietic organs, suggest only partial identity or non-identity of these two cell types. Finally it is shown that spleen colonies originating from FV-infected target cells are a primary erythroleukemic lesion, since they contain more Ep-independent CFU-E than do intercolony areas of the spleen.

Animals↗

PubMed1976

Premature chromosome condensation in human leukemia.

Premature chromosome condensation (PCC) has previously been observed in tissue culture and is believed to arise from asynchronous mitotic activity in multinucleated cells in which the affected nucleus is in interphase and at least one nucleus is in metaphase. Such cells have been noted following fusion induced by virus infection, spontaneously, and after treatment with cytochalasin B. The phenomenon has also been observed in malignant pleural effusions, but has not previously been described as a feature of hematologic disease. In this study, we report the observations of PCC in seven patients. Six of these patients had either acute myeloblastic leukemia or acute myelomonoblastic leukemia in association with the features of erythroleukemia, i.e., leukoerythroblastic reaction in the blood, and erythroid multinuclearity, "megaloblastoid" changes, and PAS-positive staining of erythroid precursor cells in the bone marrow. In all patients, erythroid multinuclearity has been noted. However, not all patients with erythroleukemia exhibit PCC. In this series, three additional patients have had similar bone marrow morphologic changes without PCC. The finding of PCC in erythroleukemia may have important implications as to etiology of this disorder.

Aged↗

PubMed1989

The regulation of erythropoiesis in man.

The physiological role of erythropoietin (epo) as a "maintenance" and "progression" factor of terminal erythroid maturation is well established. The role of early acting erythroid factors in the maintenance of steady state erythropoiesis has not been ascertained. Primitive erythroid precursor cells (burst forming units) require a biological activity for colony formation in culture, which has been designated burst promoting activity (BPA) before it became clear that granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin 3 (IL-3) are (probably among others) important components of "BPA". Unlike epo, neither GM-CSF nor IL-3 have been detected in the circulation in sufficient amounts to allow recognition of feed back mechanisms between failing erythropoiesis and either of the two factors. Rather, GM-CSF and IL-3 may play a local role in the enhancement of erythropoiesis in the bone marrow, which is resistant to study in vivo. gamma-Interferon and transforming growth factor beta inhibit erythropoiesis in vitro. Their causative role in diseases with depressed erythropoiesis, however, is not proven.

Colony-Stimulating Factors↗

PubMed1980

Erythroid colony studies on sickle cell anemia in hypoproliferative crisis.

Bone marrow cells, peripheral blood lymphocytes, and sera from patients with sickle-cell anemia in hypoproliferative crisis were studied in the plasma clot culture system in the presence or absence of erythropoietin (Epo). Bone marrow cells from five patients demonstrated a marked ability to form erythroid colonies in the presence of Epo. These studies also suggested that bone marrow cells from some patients may have an increased sensitivity to Epo. The most outstanding observation in the present study was the marked erythroid colony inhibition by serum taken from one patient during crisis. Serum taken from the same patient two months after hypoproliferative crisis had no suppressive effect on erythroid colony formation. Lymphocytes taken from three patients in crisis had a stimulatory effect on erythroid colony formation when included in culture. The conclusion is that the defect of erythropoiesis in sickle-cell anemia during hypoproliferative crisis is not due to the absence of erythroid precursor cells or to the presence of suppressor lymphocytes, but may in some cases be associated with a circulating inhibitor of erythroid maturation.

Anemia, Sickle Cell↗

PubMed1991

Reversible pure red cell aplasia associated with diphenylhydantoin therapy.

Pure red cell aplasia (PRCA) is characterised by an anaemia with reticulocytopenia but with normal leukocyte and platelet counts, and a bone marrow with the selective absence of erythroid precursor cells. Drug-induced PRCA is a rare cause of secondary erythroid aplasia, but distinct from the primary and most secondary forms, it is usually acute and fully reversible upon withdrawal of the causative drug. We report a 36 year-old Chinese man who developed diphenylhydantoin associated PRCA two months after commencing the treatment. Reappearance of reticulocytes was observed six days following the cessation of diphenylhydantoin therapy and the haemoglobin level rose to normal one month later. The extreme rarity of this adverse reaction to a drug used so widely strongly suggests an individual predisposition.

Adult↗

PubMed1978

Studies on the target cell for the Friend virus (FV-P strain) using the CFU-E technique.

In order to characterize the target cell for the polycythemia inducing Friend virus (FV-P) in vivo, mice were treated by induction of plethorism, bleeding, Actinomycin D, and Busulfan before virus infection. The development of the Friend leukemia was then studied mainly using the CFUE technique for erythroid colony growth in vitro. This technique allows the quantification of a new cell type, an erythropoietin (Ep) independent colony forming cell. These Ep independent colonies were taken as marker for the disease. Their number with time after infection was correlated with the compartment size of pluripotent, granuloid committed and erythroid stem cells at the time of infection. The results indicate that the development of the Friend leukemia does not require the actual presence of CFUE, as seen using Actinomycin D, and is not correlated with the number of pluripotent or granuloid stem cells, as seen after Busulfan. It is, however, dependent on the erythropoietic state of the animal, as seen in plethoric mice and mice after bleeding. It is, therefore, concluded that the target cell for FV-P is located within the Ep-responsive cell compartment, between early (BFUE) and late (CFUE) erythroid precursor cells.

Animals↗

PubMed2000

CDP/Cut DNA binding activity is down-modulated in granulocytes, macrophages and erythrocytes but remains elevated in differentiating megakaryocytes.

DNA binding by the CCAAT-displacement protein, the mammalian homologue of the Drosophila melanogaster Cut protein, was previously found to increase sharply in S phase, suggesting a role for CDP/Cut in cell cycle progression. Genetic studies in Drosophila indicated that cut plays an important role in cell-type specification in several tissues. In the present study, we have investigated CDP/Cut expression and activity in a panel of multipotent hematopoietic cell lines that can be induced to differentiate in vitro into distinct cell types. While CDP/Cut DNA binding activity declined in the pathways leading to macrophages, granulocytes and erythrocytes, it remained elevated in megakaryocytes. CDP/Cut was also highly expressed in primary megakaryocytes isolated from mouse, and some DNA binding activity could be detected. Altogether, these results raise the possibility that CDP/Cut may be a determinant of cell type identity downstream of the myelo-erythroid precursor cell. Another possibility, which does not exclude a role in lineage identity, is that CDP/Cut activity in megakaryocytes is linked to endomitosis. Indeed, elevated CDP/Cut activity in differentiating megakaryocytes and during the S phase of the cell cycle suggests that it may be required for DNA replication.

Animals↗

PubMed2006

Blood smear from a cat: features to "dys"cover.

A 4-year-old, spayed female, domestic shorthair cat was presented for lethargy, nonregenerative anemia, and inappetence. Results of a CBC included macrocytic, normochromic, nonregenerative anemia and a glucocorticoid-associated leukogram. On blood smear examination, neutrophils had abnormal features including hyposegmentation and a diffuse chromatin pattern with nuclear filament formation and nuclear blebbing. Microscopic examination of a roll preparation of bone marrow revealed hypolobulated megakaryocytes with asynchronous maturation of nuclei. The granulocytic to erythrocyte (G:E) ratio was 76. Segmented neutrophils had asynchronous maturation and dysplastic features. The entire erythroid lineage was markedly decreased for the degree of anemia and rare dysplastic features were noted in erythroid precursor cells. The interpretation of bone marrow findings was erythroid hypoplasia, megakaryocytic dysplasia, and granulocytic hyperplasia with dysplasia. Histopathologic examination of a bone marrow core sample also revealed myeloid hyperplasia and erythroid hypoplasia. The result of a direct immunofluorescence assay for FeLV performed on the bone marrow roll preparation was positive. A diagnosis of dysmyelopoiesis associated with FeLV infection was made. This case was unique in that the dysplastic changes occurred in cell lines that did not have associated cytopenias. The dysmyelopoiesis most closely resembled myelodysplastic syndrome with refractory cytopenia (MDS-RC); however, secondary dysmyelopoiesis could not be ruled out.

Animals↗

PubMed1980

Tumor promoters enhance myeloid and erythroid colony formation by normal mouse hemopoietic cells.

The diterpene tumor promoters enhance the proliferation in culture of myeloid and erythroid precursor cells from normal mouse hemopoietic tissues. The effect is observed only with those diterpenes that are tumor promoters, including 12-O-tetradecanoylphorbol 13-acetate (TPA); diterpenes that are inactive as tumor promoters are ineffective as stimulators of colony formation. Tumor promoters act synergistically with suboptimal concentrations of conditioned medium used as a source of colony-stimulating factor (CSF) to increase both the number and size of myeloid colonies. Formation of myeloid colonies is stimulated by tumor promoters even without addition of CSF. Both pure and mixed granulocyte/macrophage colonies develop; high concentrations (> 100 micrograms/ml) of TPA are more favorable for macrophage colony formation. In erythropoietin-stimulated cultures, tumor promoters enhance the development of relatively early and intermediate of erythroid precursors, whereas later erythroid precursors are unaffected.

Animals↗

PubMed1979

5-fluorocytosine: inhibition of hematopoiesis in vitro and reversal of inhibition by uracil.

The in vitro effect of 5-fluorocytosine on human and murine hematopoiesis was studied by means of soft-gel assays for erythroid and myeloid colony-forming cells. The drug consistently inhibited colony formation by granulocyte-monocyte and erythroid precursor cells. Clear effects were observable at concentrations of 5-fluorocytosine of 5 x 10(-5) M (6.5 micrograms/ml), and concentrations of 5 x 10(-4) M (65 micrograms/ml) caused approximately 90% inhibition of cloning of bone marrow myeloid colony-forming cells from mice and normal humans. Greater concentrations of 5-fluorocytosine were required to inhibit erythroid progenitors than to inhibit myeloid precursors. Uracil competitively reversed the toxicity of 5-fluorocytosine. Our data strongly suggest that the hematopoietic toxicity of 5-5-fluorocytosine is mediated through cellular metabolism of the drug. The reversal of mammalian, but not of fungal, cytotoxic effects of 5-fluorocytosine by uracil may have important clinical applications.

Animals↗

PubMed1982

Glucocorticoids inhibit the growth of murine fetal liver erythroid burst-forming cells.

The effects of glucocorticoids on the formation of large colonies of erythroid cells, termed "bursts," by erythroid burst-forming units (BFU-E) obtained from murine fetal liver were studied in plasma clot cultures. Fetal liver erythroid progenitor cells formed a reduced number of erythroid bursts when cultured for 9 days in the presence of dexamethasone. Similar results were obtained with other glucocorticoids, including corticosterone, cortisol, prednisone, prednisolone, and 9 alpha-fluorocortisol; in contrast, neither 11 alpha-cortisol, tetrahydrocortisol, nor progesterone influenced erythroid burst formation. Erythroid burst formation was also decreased by the addition of dexamethasone on days 5, 7, and 9 to developing erythroid bursts, indicating that the growth of BFU-E-derived erythroid precursor cells was also reduced by the glucocorticoid. The formation of erythroid bursts by murine fetal liver cells was also reduced when the cells were incubated with dexamethasone (10(-7) and 10(-8) M) for 1 h, washed, and cultured in plasma clots; the concentration of dexamethasone was reduced by the washes to levels which do not inhibit the growth of BFU-E derived erythroid progenitor cells. Similar results were obtained with various other glucocorticoids (10(-7) M). These studies demonstrate that glucocorticoids exert a suppressive effect on the formation of erythroid bursts by murine fetal liver erythroid progenitor cells, and that this effect is the net result of inhibitory effects on the BFU-E and its progeny.

Animals↗

PubMed1990

Role of erythropoietin in adaptation to hypoxia.

The glycoprotein hormone erythropoietin (EPO) counteracts tissue hypoxia by increasing the systemic oxygen-carrying capacity. It induces augmentation of red blood cell mass by stimulating the formation and differentiation of erythroid precursor cells in the bone marrow. EPO production is increased under various forms of diminished oxygen supply such as anemic or hypoxic hypoxia. In the adult organism, the kidneys are the major source of EPO. The precise nature of the cells responsible for renal EPO production, however, has not yet been elucidated. Most likely, peritubular cortical cells, e.g. interstitial or endothelial cells, are involved in the elaboration of the hormone. From the observation that isolated perfused rat kidneys produce EPO in an oxygen-dependent fashion we conclude that the 'oxygen sensor' that controls hypoxia-induced EPO synthesis is located in the kidney itself. Within the kidneys, the local venous oxygen tension which reflects the ratio of oxygen supply to oxygen consumption is measured and transformed into a signal that regulates the formation of EPO. However, the mechanism by which a decrease of oxygen delivery to the kidneys is linked to an enhanced EPO gene expression is not yet known. Two possible mechanisms of regulation are discussed: First, renal hypoxia could lead to enhanced formation of metabolic mediators, for example prostaglandins or adenosine, which might stimulate EPO gene transcription by increasing cellular levels of second messenger molecules. Second, some kind of molecular 'oxygen receptor' such as a heme protein, that controls EPO formation by an oxygen-dependent conformational change, could mediate signal transduction.

Animals↗

PubMed1983

Monoclonal antibody against human macrophages/monocytes and granulocytes.

A monoclonal antibody of the IgG2a isotype directed against lymphokine-activated human macrophage cell line (U937) was produced and characterized. By indirect immunofluorescence microscopy or binding assay, this antibody (MaG-1) reacted with human peripheral monocytes, peritoneal macrophages, alveolar macrophages, and peripheral granulocytes but not with lymphocytes, erythrocytes, and platelets. MaG-1 antigen was also expressed by 34% of bone-marrow cells which includes monocytic and granulocytic precursors, whereas lymphoid and erythroid precursor cells were found on MaG-1 negative population. Immunoprecipitation of 125I-labeled U937 cell extract with the Mag-1 antibody under nonreducing and reducing conditions yielded a specific band of 66 kD. Thus, this antibody defines a new human macrophage/monocyte and granulocyte-specific antigen and may be useful for studying differentiation of human macrophages/monocytes.

Antibodies, Monoclonal↗

PubMed1977

The effects of red blood cell extracts on the proliferation of erythrocyte precursor cells, in vivo.

Saline incubation extracts of mature erythrocytes were assayed in vivo by a variety of techniques in order to study their ability to modify the proliferation of maturing erythroid cells. Using comparable extracts from granulocytes and lymphocytes, the specificity of the effect of the red cell extract for erythroid cells was confirmed by measurement of autoradiographic labelling indices, radio-iron incorporation and spleen colony growth. The erythroid cells were found to be very sensitive to the effects of the extract, as little as 10 microgram per mouse producing a maximum effect on iron incorporation. It was found that the extract does not block erythroid cells proliferation completely but simply lengthens the cell cycle, mainly by increasing the GI phase of the cycle. There was no effect on the committed erythroid precursor cells. The in vivo activity, specificity and non-toxicity to the cells, together with the cells' sensitivity to red cell extract suggest, therefore, that this inhibitor may play a physiological role in the control of red cell production.

Anemia↗

PubMed1985

Drug-induced agranulocytosis: evidence for the commitment of bone marrow haematopoiesis.

Clinical and haematological features of 61 patients with drug-induced agranulocytosis (63 episodes) are presented. Multiple drug consumption was a common observation and complicated the attempt to incriminate a particular drug as being aetiologically involved. Bone marrow analysis shortly after the diagnosis revealed evidence for an impairment of proliferative granulopoiesis in the majority of cases. This observation was confirmed by in vitro culturing of granuloid precursor cells (CFU-c). Moreover, the data clearly demonstrated that drug-induced agranulocytosis may not be restricted to the granulocytic series. Thrombocytosis and reticulocytosis during the recovery phase are taken as an indication for the commitment of all haemopoietic cell lineages in agranulocytosis. These observations were in accordance with cytomorphological studies and in vitro culture data of erythroid precursor cells (CFU-e, BFU-e) of bone marrow aspirates taken in the initial phase of agranulocytosis. More than 25% of the patients showed a marked erythroid depression in the marrow.

Adolescent↗