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Fetal compensation of the hemolytic anemia in mice homozygous for the normoblastosis (nb) mutation.

The mouse autosomal recessive mutation nb causes a deficiency of erythroid ankyrin and generates a life-threatening hemolytic anemia in adult mice; however, at birth, nb/nb mice appear to be robust and show no pallor. In our study, the time of disease onset was sought by comparison of nb/nb and +/? mice both in utero and postnatally. Erythroid ankyrin messenger RNA (mRNA) is expressed in fetal erythroid progenitors from normal mice, but is reduced to 10% of normal levels in mutant fetuses. Despite the deficiency of erythroid ankyrin mRNA, 16 and 18 day nb/nb fetuses have normal levels of red blood cells (RBCs) and the RBCs are morphologically normal by scanning electron microscopy. The earliest signs of any clinical anomaly are an increase in the number of circulating reticulocytes and the deposition of minor amounts of iron just before birth in the 18 day fetal nb/nb liver, suggesting that RBCs are being destroyed. Within 24 hours after birth, nb/nb neonates have a slight but significant decrease of their RBC counts. During the next 5 days, the nb/nb RBC counts decrease markedly, the reticulocyte counts assume the mutant adult levels of 60%, the erythrocytes become microcytic and fragmented, and iron deposits accumulate in the liver. The rapid onset of clinical disease postnatally, coupled with our findings that the erythroid ankyrin gene is transcribed in fetal erythroid cell precursors from normal mice, suggest that mechanisms exist in the nb/nb fetus to compensate for the erythroid ankyrin deficiency.

Aging↗

Changes in globin messenger RNA content during erythroid cell differentiation.

Previous studies have shown that mouse fetal erythroid precursor cells isolated by an immunological technique synthesize little or no globin and contain little, if any, globin mRNA, as assayed in a cell-free system (translatable mRNA). After culture for 10 hours in the presence of erythropoietin, there is a marked increase in globin synthesis and in translatable globin mRNA. The present studies were designed to measure directly the content of globin mRNA sequences during erythroid cell differentiation, by molecular hybridization with 3H-labeled DNA complementary to globin mRNA. The results indicate that few, if any, globin mRNA sequences are present in the total RNA of erythroid precursor cells. There is little or no pool of untranslated globin mRNA in these cells. After 10 hours of culture with erythropoietin, there is an increase in globin mRNA content, as ;easured by a change in the Cot1/2 values obtained by cDNA: mRNA hybridization with (Co) representing the concentration of RNA. Between 0 and 22 hours of culture, there is a 250-fold rise, and between 22 and 44 hours, a further 2-fold increase in globin mRNA content. During the 44 hours in culture, the number of cells in culture increases 2- to 3-fold. The number of globin mRNA molecules rises in erythroid precursor cells to an average value of 1800 molecules/cell during 22 hours of culture. In cultures without added erythropoietin, the absolute number of cells decreases, however, cells presumably induced to differentiate by exposure to erythropoietin in vivo continue to differentiate in vitro, accumulating globin mRNA and initiating globin synthesis.

Animals↗

Adducin in erythrocyte precursor cells of rats and humans: expression and compartmentalization.

Adducin is a calmodulin-binding protein involved in the assembly of the erythrocyte membrane skeleton. To investigate the expression of adducin during human erythropoiesis, we performed immunofluorescence studies on smears of cultured human erythroblasts. Adducin immunoreactivity was found in the early stages of erythropoiesis. Proerythroblasts were the first erythroid precursor cells positive for adducin. The adducin signal was very similar to the signal of erythroid beta-spectrin in that both proteins lined the membrane of erythroid precursor cells. Cell fractionation experiments were performed to further analyze the intracellular distribution of adducin in erythroid cells. In erythroblasts, about 60% of total cellular adducin appeared in the Triton-soluble fraction. In reticulocytes, the Triton-soluble fraction decreased to 30% of total reticulocyte adducin. Erythrocytes had no detectable amount of adducin in the Triton-soluble pool. Instead, adducin was quantitatively bound to the Triton-insoluble erythrocyte cytoskeleton. Our results suggest that adducin is expressed early in the development of the erythrocyte membrane skeleton, whereas stable assembly onto the membrane skeleton does not occur before the final stages of mammalian erythropoiesis.

Animals↗

Autocrine differentiation-inhibiting factor (ADIF) from chicken erythroleukemia cells acts on human and mouse early BFU-E erythroid progenitors.

tsAEV-LSCC HD3 chicken erythroid cells transformed by the avian erythroblastosis virus (AEV) secrete an autocrine differentiation-inhibiting factor, ADIF, which blocks differentiation without affecting proliferation of the chicken erythroid cells that synthesize and secrete it into the culture medium. The chicken erythroleukemia cell ADIF activity is not restricted to avians. It prevents dimethylsulfoxide (DMSO) from stimulating murine Friend erythroleukemia cells to synthesize hemoglobin. ADIF also blocks erythroid differentiation in normal human and murine bone marrow where it selectively targets the early BFU-E (burst-forming) erythroid precursor cells without affecting the more advanced CFU-E erythroid precursor cells or cells of the different granulocyte-macrophage lineage.

Animals↗

Parvovirus B19-induced perturbation of human megakaryocytopoiesis in vitro.

Parvovirus B19 infection leads to transient aplastic crises in individuals with chronic hemolytic anemias or immunodeficiency states. An additional unexplained sequela of B19 infection is thrombocytopenia. Because B19 is known to have a remarkable tropism for human erythropoietic elements, and is not known to replicate in nonerythroid cells, the etiology of this thrombocytopenia is uncertain. We sought to define the pathobiology of B19-associated thrombocytopenia by examining the role of B19 on in vitro megakaryocytopoiesis. B19 infection of normal human bone marrow cells significantly suppressed megakaryocyte (MK) colony formation compared with mock-infected cells. No such inhibition was observed with a nonpathogenic human parvovirus, the adeno-associated virus 2 (AAV). The B19-MK cell interaction was also studied at the molecular level. Whereas low-density bone marrow cells containing erythroid precursor cells supported B19 DNA replication, no viral DNA replication was observed in B19-infected MK-enriched fractions as determined by the presence of viral DNA replicative intermediates on Southern blots. However, analysis of total cytoplasmic RNA isolated from B19-infected MK fractions showed a low-level expression of the B19 genome as detected by quantitative RNA dot blots as well as by Northern analysis. Furthermore, a frame-shift mutation in a recombinant AAV-B19 hybrid genome segment that encodes the viral nonstructural (NS1) protein significantly reduced the observed inhibition of MK colony formation. These studies indicate tissue-tropism of B19 beyond the erythroid progenitor cell, and lend support to the hypothesis that B19 genome expression may be toxic to cell populations that are nonpermissive for viral DNA replication.

Blotting, Northern↗

Na pump isoforms in human erythroid progenitor cells and mature erythrocytes.

This study is aimed at identifying the Na pump isoform composition of human erythroid precursor cells and mature human erythrocytes. We used purified and synchronously growing human erythroid progenitor cells cultured for 7-14 days. RNA was extracted from the progenitor cells on different days and analyzed by RT-PCR. The results showed that only the alpha1, alpha3, beta2, and beta3 subunit isoforms and the gamma modulator were present. Northern analysis of the erythroid progenitor cells again showed that beta2 but not beta1 or alpha2 isoforms were present. The erythroid cells display a unique beta subunit expression profile (called beta-profiling) in that they contain the message for the beta2 isoform but not beta1, whereas leukocytes and platelets are known to have the message for the beta1 but not for the beta2 isoform. This finding is taken to indicate that our preparations are essentially purely erythroid and free from white cell contamination. Western analysis of these cultured progenitor cells confirmed the presence of alpha1, alpha3, (no alpha2), beta2, beta3, and gamma together now with clear evidence that beta1 protein was also present at all stages. Western analysis of the Na pump from mature human erythrocyte ghosts, purified by ouabain column chromatography, has also shown that alpha1, alpha3, beta1, beta2, beta3, and gamma are present. Thus, the Na pump isoform composition of human erythroid precursor cells and mature erythrocytes contains the alpha1 and alpha3 isoforms of the alpha subunit, the beta1, beta2, and beta3 isoforms of the beta subunit, and the gamma modulator.

Cells, Cultured↗

Benzene induces gene-duplicating but not gene-inactivating mutations at the glycophorin A locus in exposed humans.

Occupational exposure to benzene is known to cause leukemia, but the mechanism remains unclear. Unlike most other carcinogens, benzene and its metabolites are weakly or nonmutagenic in most simple gene mutation assays. Benzene and its metabolites do, however, produce chromosomal damage in a variety of systems. Here, we have used the glycophorin A (GPA) gene loss mutation assay to evaluate the nature of DNA damage produced by benzene in 24 workers heavily exposed to benzene and 23 matched control individuals in Shanghai, China. The GPA assay identifies stem cell or precursor erythroid cell mutations expressed in peripheral erythrocytes of MN-heterozygous subjects, distinguishing the NN and N phi mutant variants. A significant increase in the NN GPA variant cell frequency (Vf) was found in benzene-exposed workers as compared with unexposed control individuals (mean +/- SEM, 13.9 +/- 1.7 per million cells vs. 7.4 +/- 1.1 per million cells in control individuals; P = 0.0002). In contrast, no significant difference existed between the two groups for the N phi Vf (9.1 +/- 0.9 vs. 8.8 +/- 1.8 per million cells; P = 0.21). Further, lifetime cumulative occupational exposure to benzene was associated with the NN Vf (P = 0.005) but not with the N phi Vf (P = 0.31), suggesting that NN mutations occur in longer-lived bone marrow stem cells. NN variants result from loss of the GPA M allele and duplication of the N allele, presumably through recombination mechanisms, whereas NO variants arise from gene inactivation, presumably due to point mutations and deletions. Thus, these results suggest that benzene produces gene-duplicating mutations but does not produce gene-inactivating mutations at the GPA locus in bone marrow cells of humans exposed to high benzene levels. This finding is consistent with data on the genetic toxicology of benzene and its metabolites and adds further weight to the hypothesis that chromosome damage and mitotic recombination are important in benzene-induced leukemia.

Adolescent↗

An epidemiologic study of early biologic effects of benzene in Chinese workers.

Benzene is a recognized hematotoxin and leukemogen, but its mechanisms of action in humans are still uncertain. To provide insight into these processes, we carried out a cross-sectional study of 44 healthy workers currently exposed to benzene (median 8-hr time-weighted average; 31 ppm), and unexposed controls in Shanghai, China. Here we provide an overview of the study results on peripheral blood cells levels and somatic cell mutation frequency measured by the glycophorin A (GPA) gene loss assay and report on peripheral cytokine levels. All peripheral blood cells levels (i.e., total white blood cells, absolute lymphocyte count, platelets, red blood cells, and hemoglobin) were decreased among exposed workers compared to controls, with the exception of the red blood cell mean corpuscular volume, which was higher among exposed subjects. In contrast, peripheral cytokine levels (interleukin-3, interleukin-6, erythropoietin, granulocyte colony-stimulating factor, tissue necrosis factor-alpha) in a subset of the most highly exposed workers (n = 11) were similar to values in controls (n = 11), suggesting that benzene does not affect these growth factor levels in peripheral blood. The GPA assay measures stem cell or precursor erythroid cell mutations expressed in peripheral red blood cells of MN heterozygous subjects, identifying NN variants, which result from loss of the GPA M allele and duplication of the N allele, and N phi variants, which arise from gene inactivation. The NN (but not N phi) GPA variant cell frequency was elevated in the exposed workers compared with controls (mean +/- SD, 13.9 +/- 8.4 mutants per million cells versus 7.4 +/- 5.2 per million cells, (respectively; p = 0.0002), suggesting that benzene produces gene-duplicating but not gene-inactivating mutations at the GPA locus in bone marrow cells of exposed humans. These findings, combined with ongoing analyses of benzene macromolecular adducts and chromosomal aberrations, will provide an opportunity to comprehensively evaluate a wide range of early biologic effects associated with benzene exposure in humans.

Adult↗

NTP technical report on the toxicity studies of a Chemical Mixture of 25 Groundwater Contaminants Administered in Drinking Water to F344/N Rats and B6C3F(1) Mice.

Toxicity studies were performed with a chemically defined mixture of 25 groundwater contaminants, using dose levels considered to have environmental relevance. The mixture contained 19 organic compounds and six metals (shown below); the selection of these compounds was based primarily on the frequency of their occurrence in United States Environmental Protection Agency surveys of groundwater contamination in the vicinity of hazardous waste disposal sites. This report focuses primarily on 26-week drinking water toxicity studies with male and female F344/N rats and B6C3F(1) mice. The endpoints evaluated included histopathology, clinical pathology, neurobehavioral studies, and reproductive toxicity. Additional studies using this same chemical mixture are briefly reviewed in this report and include an evaluation of spermatogenesis in B6C3F(1) mice exposed to the chemical mixture for 13 weeks, a continuous breeding study with Sprague-Dawley rats and CD-1(R) Swiss mice, studies of myelotoxicity in B6C3F(1) mice exposed to the chemical mixture for up to 31.5 weeks, studies of immunosuppression in B6C3F(1) mice exposed for up to 13 weeks, in vitro mutagenicity assays in Salmonella typhimurium and Escherichia coli, and measures of genetic damage in bone marrow and peripheral blood of F344/N rats and B6C3F(1) mice in 2-week drinking water studies. In a 26-week drinking water study in which rats were administered the chemical mixture at composite contaminant concentrations of 0, 11, 38, 113, or 378 ppm, no deaths occurred and the body weight gain of high-dose males was slightly less than that of the controls. Water consumption decreased with dose and was 24% to 28% less than that of the controls at the highest concentration. Changes in organ weights occurred primarily in high-dose rats and included increased absolute and relative liver and kidney weights in females, increased relative kidney weight in males, and decreased absolute and relative thymus weights in males and females. Hematologic assessments indicated that rats receiving 378 ppm developed a microcytic anemia consistent with that accompanying iron depletion. Multiple foci of inflammation occurred in the liver of exposed rats. In high-dose females, these liver lesions were especially prominent and included bile duct and oval cell hyperplasia. Inflammation also occurred in the mesenteric lymph nodes, the adrenal gland, and the spleen. The amount of hemosiderin in the spleens of rats receiving the higher concentrations of the chemical mixture was less than normal. Components of a chemical mixture of 25 groundwater contaminants include acetone, aroclor 1260, arsenic, benzene, cadmium, carbon tetrachloride, chlorobenzene, chloroform, chromium, 1,1-dichloroethane, 1,2-dichloroethane, 1,1-dichloroethylene, 1,2-trans-dichloroethylene, di(2-ethylhexyl) phthalate, ethylbenzene, lead, mercury, methylene chloride, nickel, phenol, tetrachloroethylene, toluene, 1,1,1-trichloroethane, trichloroethylene, xylenes. In a 26-week study in which mice were exposed to the chemical mixture at concentrations of 0, 11, 38, 113, and 378 ppm in drinking water, there were no clear adverse effects noted in survival, weight gain, clinical pathology parameters, or histopathologic evaluations. Water consumption decreased with increasing dose, and water consumption by high-dose mice was approximately 40% less than that by the controls. In neurobehavioral assessments, no clear treatment-related effects were observed in measures of forelimb and hindlimb grip strength, hindlimb footsplay, motor activity, response to a thermal stimulus, or startle response in rats or mice evaluated at 6-week intervals throughout the 26- week drinking water studies. There were no effects on sperm morphology or motility or on estrous cycle length in rats or mice receiving the chemical mixture during the 26-week studies. Sperm concentration was decreased in F(1) CD-1(R) Swiss mice during continuous breeding studies, although there were no clear adverse effects on the fertility of Sprague-Dawley rats or CD-1(R) Swiss mice in th CD-1® Swiss mice in these studies. Pup weight, the number of live males, and the number of male pups per litter were slightly decreased in dosed rats in the continuous breeding study in rats; the number of live female mouse pups in litters born of the F(0) and F(1) generations was decreased in the 378 ppm group. The significance of these observations, if any, is not known. F(1) mice receiving 378 ppm had increased incidences of hepatic inflammation compared to the controls. In female B6C3F(1) mice that received the chemical mixture in drinking water at concentrations as high as 756 ppm for 2 weeks or 378 ppm for 13 weeks, assessments of immune function showed suppression of hematopoietic stem cells and antigen-induced antibody-forming cells. This was manifested by impaired resistance to challenge with a nonlethal strain of mouse malaria, Plasmodium yoelii. Additional evidence of an adverse effect on hematopoietic stem cells was demonstrated by decreases in the in vitro colony-forming ability of granulocyte-macrophage progenitor cells and erythroid precursor cells isolated from female mice that had received the chemical mixture at a concentration of 378 or 756 ppm in 31.5 week studies. Potential genotoxic effects of the chemical mixture to the bone marrow of F344/N rats and B6C3F(1) mice were assessed in 2-week drinking water studies with concentrations as high as 756 ppm. Small increases in sister chromatid exchanges and micronucleated polychromatic erythrocytes occurred in the bone marrow of dosed male mice, and micronucleated polychromatic erythrocytes were also increased in dosed female mice. The chemical mixture did not induce mutations in Salmonella typhimurium strains TA98 and TA100 and did not induce DNA damage in Escherichia coli with or without metabolic activation. In summary, rats receiving drinking water containing a mixture of 25 common groundwater contaminants at levels of potential environmental relevance developed inflammatory lesions in the liver, spleen, lymph nodes, and adrenal gland, as well as evidence of an iron deficiency anemia. The inflammatory lesions could not be predicted based on the known toxic effects of the individual components of the chemical mixture. Mice exposed to similar concentrations of the chemical mixture did not show adverse effects in a standard toxicity study but developed deficits in bone marrow function, evidence of genetic damage, hepatic inflammation, and immunosuppression in other studies that generally included exposures to higher concentrations or exposures of longer duration. A no-observed-adverse-effect level for histologic injury (granulomatous inflammation of the liver) was 11 ppm in rats; however, no clear evidence for histologic injury was seen in mice exposed to concentrations of the chemical mixture as high as 378 ppm in a standard 26-week study. NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.

Journal Article↗

Isolation of erythropoietin-sensitive cells from Friend virus-infected marrow cultures: characteristics of the erythropoietin response.

Murine erythroid precursor cells, stimulated to proliferate in vitro in the absence of added erythropoietin (EP) by the anemia strain of Friend virus (FVA), will subsequently respond to EP by complete erythrocyte differentiation. If not exposed to EP, the erythroid cells divide for about 120 hr in culture, and they maintain the potential for full differentiation in response to EP added at any time during the period from 72 to 120 hr. Between 96 and 120 hr of culture without added EP, the EP-sensitive erythroid precursor cells that have formed discrete erythroid bursts can be isolated in relatively large numbers from such cultures by plucking with a Pasteur pipette. The addition of EP initiates the final stages of erythroid differentiation, including heme synthesis in 70%-80% of these isolated cells. With respect to homogeneity of the precursor cells, quantity of EP-responsive cells obtainable, and uniformity of EP responsiveness, this system is uniquely favorable for biochemical studies of the late differentiation effects of EP. The overall changes in gene expression accompanying EP-induced terminal differentiation were examined by two-dimensional gel electrophoresis of proteins labeled for a short time with radioactive amino acids. Several new proteins are synthesized in these erythroid cells during terminal differentiation, but the number is a very small percentage of the total number of proteins being made. Thus, in this system, the effect of EP is to initiate expression of a small group of genes, including those for globins, spectrin, and other proteins involved in the final stages of erythroid differentiation.

Animals↗

Multiple members of the TNF superfamily contribute to IFN-gamma-mediated inhibition of erythropoiesis.

IFN-gamma inhibits the growth and differentiation of erythroid precursor cells and mediates hemopoietic suppression through mechanisms that are not completely understood. We found that treatment of human erythroid precursor cells with IFN-gamma up-regulates the expression of multiple members of the TNF family, including TRAIL and the recently characterized protein TWEAK. TWEAK and its receptor fibroblast growth factor-inducible 14 (Fn14) were expressed by purified erythroblasts at all the stages of maturation. Exposure to recombinant TWEAK or agonist anti-Fn14 Abs was able to inhibit erythroid cell growth and differentiation through caspase activation. Because other members of the TNF family such as TRAIL and CD95 ligand (CD95L) are known to interfere with erythroblast growth and differentiation, we investigated the role of different TNF/TNFR family proteins as potential effectors of IFN-gamma in the immature hemopoietic compartment. Treatment of erythroid precursor cells with agents that blocked either TRAIL, CD95L, or TWEAK activity was partially able to revert the effect of IFN-gamma on erythroid proliferation and differentiation. However, the simultaneous inhibition of TRAIL, TWEAK, and CD95L resulted in a complete abrogation of IFN-gamma inhibitory effects, indicating the requirement of different receptor-mediated signals in IFN-gamma-mediated hemopoietic suppression. These results establish a new role for TWEAK and its receptor in normal and IFN-gamma-mediated regulation of hematopoiesis and show that the effects of IFN-gamma on immature erythroid cells depend on multiple interactions between TNF family members and their receptors.

Apoptosis Regulatory Proteins↗

Flow cytometric analysis of the association between blood group-related proteins and the detergent-insoluble material of K562 cells and erythroid precursors.

The linkage between blood group-related cell surface proteins and the detergent-insoluble material (DIM) was estimated by flow cytometry using a panel of specific monoclonal antibodies (mAbs) as a comparison of the antibody-binding capacity of intact and Triton-X100-treated cells. Studies were performed with K562 cells expressing endogenous or recombinant proteins and with human erythroid progenitors during their proliferation and differentiation in vitro. Glycophorin C (GPC) was found to be Triton-insoluble in both cellular models. When expressed (erythroid progenitors), Band 3 remained Triton-insoluble. Glycophorin A (GPA), however, behaved as Triton-soluble or insoluble according to the absence (K562) or the presence (erythroid progenitors) of Band 3 respectively. Comparison of the cellular models regarding the proteins that compose the Rh complex also indicated that Rh(D), RhAG and CD47 were resistant to Triton extraction in cells lacking Band 3. Similarly, RhAG and CD47 remained predominantly Triton-insoluble in K562 cells and early progenitors before Rh and Band 3 expression. Further analysis showed that the Kell protein was DIM-associated. In contrast, CD99 and DARC (Fy) proteins were not, or were very poorly, DIM-associated. Additionally, the adhesion molecules CD44 and Lu were completely or partially resistant to detergent extraction respectively. Deletion of the Lu cytoplasmic tail or its replacement by the cytoplasmic domain of GPC resulted in significant increase or decrease of the Triton solubility of the transfected proteins respectively. These data suggest that Triton insolubility of Lu results in part from direct attachment of its cytoplasmic tail with the cytoskeleton. We assume that this method should provide a useful tool to map interaction sites localized in the cytoplasmic domain of recombinant transmembrane proteins.

Anion Exchange Protein 1, Erythrocyte↗

Selection against blood cells deficient in hypoxanthine phosphoribosyltransferase (HPRT) in Lesch-Nyhan heterozygotes occurs at the level of multipotent stem cells.

Lesch-Nyhan syndrome is caused by a severe genetic deficiency of hypoxanthine phosphoribosyltransferase (HPRT) and is characterized by central nervous system disorders, gout, and in some cases, macrocytic anemia. Women heterozygous for HPRT deficiency are healthy but their somatic cells are mosaic for enzyme deficiency owing to random inactivation of the X chromosome. Frequencies of red blood cells and T cells deficient in HPRT are significantly lower than the expected 50% in heterozygotes, suggesting that HPRT-negative blood cells are selected against in heterozygotes. To determine at which stage of hematopoiesis such selection occurs, we determined the frequencies of HPRT-negative T, B and erythroid precursor cells in three heterozygotes. Since the cloning efficiencies of T and B cells and colony forming efficiency of burst-forming unit erythroid (BFU-E) for sample from Lesch-Nyhan patients were similar to those of normal cells, HPRT deficiency does not seem to render the differentiated cells less efficient for proliferation. However, the frequencies of HPRT-negative T and B cells, and BFU-E were all less than 10% in each of the three heterozygotes. Although the frequencies of HPRT-negative cells showed tenfold variations between the heterozygotes, each heterozygote had similar frequencies of HPRT-negative cells in the three cell types. These results suggest that HPRT is important at early stages of hematopoiesis, but less so after the cells have differentiated into T cells, B cells and erythroid precursor cells.

Adult↗

Parmacological regulation of erythropoietic precursor pool in experimental neuroses.

We studied the effect of bone marrow Thy 1,2+ cells on the growth of erythroid colonies and the role of monoamine in the regulation of proliferation and differentiation of erythroid precursor cells in experimental neuroses. Under conditions of conflict situation Thy 1,2+ cells stimulated the growth of erythropoietic precursors (directly and via interaction with adherent cells of the hemopoiesis-inducing environment). Under conditions of paradoxical sleep deprivation the absence of interaction between Thy 1,2+ cells and adherent bone marrow fraction disturbs erythroid colony formation. In experimental neuroses the state of erythropoietic precursors and secretory activity of elements of the hemopoiesis-inducing microenvironment are controlled by monoamines. The regulatory effect of monoamines is realized via adrenergic and erythropoietin-sensitive receptors on erythroid precursors and cells of the hemopoiesis-inducing microenvironment.

Animals↗

Gender- and age-specific cytotoxic susceptibility to benzene metabolites in vitro.

Benzene, a widely used compound, is a known carcinogen and hematopoietic toxicant. Several studies have shown gender and age differences in the responses to benzene-induced hematotoxicity. It is not known if these differences in response are due to age- or gender-associated metabolic differences or to age- or gender-associated differences in the susceptibilities of the target cells. In order to address this issue, mouse colony-forming units-erythroid (CFU-e, an erythroid precursor cell particularly susceptible to benzene toxicity) were cultured in the presence of either individual benzene metabolites or binary mixtures of these metabolites. CFU-e were obtained from unexposed age-matched adult male and female (both virgin and pregnant) Swiss Webster (SW) mice and from SW male and female 16-day fetuses. The metabolites used were phenol, hydroquinone, catechol, benzoquinone, and trans, trans-muconic acid. The concentrations of the individual metabolites used were 10, 20, and 40 microM. Binary mixtures of metabolites were prepared using the lowest concentrations of the individual metabolites that caused cytotoxicity. These concentrations were 10 microM for hydroquinone, catechol, and benzoquinone, and 40 microM for phenol and muconic acid. In general, the CFU-e from adult females (both virgin and pregnant) were more resistant to the toxic effects of the individual metabolites than CFU-e from other subjects. CFU-e from adult males were more susceptible to the cytotoxic effects of hydroquinone and benzoquinone than CFU-e from other subjects and CFU-e from both male and female fetuses were highly sensitive to the toxic effects of catechol. On the other hand, CFU-e from adult males were less susceptible to the cytotoxic effects of catechol than CFU-e from other subjects. Similar results were observed with binary mixtures of metabolites. CFU-e from adult males were more susceptible to the binary mixtures than CFU-e from virgin females and CFU-e from fetal males were more susceptible than CFU-e from fetal females. In addition, CFU-e from fetuses were more 'resistant than CFU-e from adults to the cytotoxic effects of those binary mixtures that did not contain catechol. In contrast, binary mixtures containing catechol were more toxic to fetal cells than to adult cells. These results suggest that differences in benzene hematotoxicity associated with gender and age may be due, at least in part, to intrinsic factors at the level of the target cell rather than solely to age- or gender-related differences in the metabolism of benzene.

Age Factors↗

Human thymic epithelial cells maintain long-term survival of clonogenic myeloid and erythroid progenitor cells in vitro.

Precursor cells that migrate into the thymus are still multipotent. Therefore, thymic epithelial cells (TECs) may provide microenvironments not only for T-cell development, but also for maintenance of multipotent precursor cells until they undergo T-cell commitment. In the present study, we performed long-term cultures of CD34+ bone-marrow (BM) cells on TEC lines that were derived from cortical epithelial cells of post-natal thymus, to investigate whether human TECs could maintain long-term nonlymphoid haematopoiesis. Haematopoietic cells maintained in direct contact with established TEC lines were able to generate clonogenic progeny to both myeloid and erythroid cells for periods in excess of 5 weeks. Their abilities to support colony-forming units of granulocytes-macrophages (CFU-GM) and burst-forming units of erythroids (BFU-E) were almost equal to those of BM stromal cells. We observed similar results by using cloned TEC lines derived by limiting dilution, as well as those by using parental TEC lines. Colony-forming activities were maintained even when haematopoietic progenitor cells were physically separated from TEC lines and cultured on microporous membrane. These observations indicate that haematopoiesis maintained in TEC-contact long-term cultures may depend on soluble factors produced by TEC lines. Our results suggest that thymic cortical epithelial cells have the ability to support not only the differentiation of haematopoietic cells, but also long-term survival of clonogenic myeloid/erythroid progenitor cells.

Antigens, CD34↗

Induction of pre-B lymphoid leukemia following reconstitution of lethally irradiated mice with v-erb-B virus-infected bone marrow progenitor cells.

We have previously shown that v-erb-B contained within a recombinant murine retroviral vector is capable of transforming pre-B lymphocytes (M. Miller, A. K. Kennewell, and G. Symonds, Leukemia, 6: 18-28, 1992) and early erythroid precursor cells [blast-forming units (erythroid) (M. Miller, A. Kennewell, Y. Takayama, A. Bruskin, J. M. Bishop, G. Johnson, and G. Symonds, Oncogene, 5: 1125-1131, 1990)] in vitro. To determine the sites and nature of v-erb-B-induced transformation in vivo, the hematopoietic systems of lethally irradiated mice were repopulated with v-erb-B-infected bone marrow. All mice became moribund within 4-12 weeks of reconstitution, with a median onset of disease at 6 weeks. Histopathological and flow cytometric evaluation of tissues from diseased mice, as well as morphological and phenotypic analysis (cytochemical as well as molecular) of the cell lines established from the mice, revealed that all but one of the mice examined at postmortem had developed a pre-B lymphoid leukemia or lymphoma. Abnormally high levels of mast cells in the spleen and bone marrow of the remaining mouse indicated a mast cell disease. The development of pre-B lymphoid malignancy in the majority of the reconstituted mice indicates a marked predisposition of v-erb-B to transform cells of the pre-B lymphoid lineage. The reconstitution of lethally irradiated mice with v-erb-B virus-infected bone marrow provides a model system for the analysis of events involved in the initiation and maintenance of acute lymphoid leukemia.

Animals↗

Regeneration of erythroid committed precursor cells in polycythaemic mice treated with cyclophosphamide.

The recovery of erythroid stem cells and pluripotent haemopoietic stem cells (CFUS) was estimated in mice treated with cyclophosphamide (Cy) by measuring CFUS, the erythroid repopulating ability (ERA) of bone marrow cells and erythropoietin responsive cells (ERC). The experiments were performed in hypertransfused CBA mice previously injected with 200 mg/kg Cy. CFUS, ERA and response to a single dose of erythropoietin-Ep (5 U) were measured at 24 h time intervals for 7, 4 and 8 days respectively. The proliferation rate of CFUS and erythroid repopulating cells was estimated on the basis of cytosine arabinoside (AraC) suicide data. The results obtained demonstrate that CFUS and ERA do not regenerate at the same rate. ERA recovery preceded CFUS regeneration at the time when the Ep response was depressed. The proliferation rate of CFUS decreased with regeneration of CFUS while AraC suicide of erythroid repopulating cells remained high at the time when ERA had recovered to 80% of control values.

Animals↗