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PubMed2006

Erythroid cells play essential roles in angiogenesis by bone marrow cell implantation.

Bone marrow cell implantation (BMI) has been utilized to treat patients with limb and heart ischemia. BMI provides angiogenic precursors and angiogenic cytokine-producing cells, especially erythroid cells. In this study, we induced in vitro angiogenesis cultures and in vivo BMI simulation using a murine limb ischemia model to examine the role of erythroid cells and the effect of erythropoietin (EPO). Human erythroid colonies (BFU-e) induced capillary networks around the colonies in vitro. Erythroid cells in human bone marrow produced vascular endothelial growth factor and placental growth factor. The angiogenic effects of erythroid cells were further amplified in the presence of EPO. Limb-ischemic mice were treated with BMI +/- EPO, and limb survival, blood flow recovery, and muscle histology were analyzed. Treatment with whole bone marrow cells + EPO significantly improved limb survival and blood flow. The cumulative effects of EPO on BMI induced and increase in capillary number and artery enlargement. Erythroid cells were essential for the in vivo effects of BMI, and CD14-positive cells supported the biological effects. In addition to the direct effect of EPO on angiogenesis, EPO showed indirect effect on angiogenesis through amplifying the angiogenic effects by erythroid cells supported by CD14-positive cells.

Adult↗
PubMed2002

No apoptotic cell death of erythroid cells of erythroblastic islands in bone marrow of healthy rats.

A possibility of apoptotic cell death in erythropoietic regulation was examined by means of detailed light microscopical histoplanimetry, electron microscopy, the in situ nick-end labeling method, and an immunohistological method in the rat bone marrow. Serum erythropoietin concentrations were shown at normal levels. The erythroid series on a mature process presented several morphological features of apoptosis, i.e. the shrinkage of both nuclei and cytoplasm and the chromatin condensation. In the light microscopical histoplanimetry, however, morphological signs of final apoptotic cell death were never found in any erythroid cell within the erythroblastic islands. This finding was also supported by detailed ultrastructural observation: No erythroid cell bodies were trapped and degraded by the central macrophages of the erythroblastic islands, while the denucleated nuclei with small amount of cytoplasm of late erythroblasts were often trapped and degraded in the macrophages. Nuclear DNA fragmentation was not detected in any erythroblasts, but was detected in the lysosomes of the central macrophages. These findings suggest that erythropoiesis is regulated by other regulatory mechanisms than apoptotic cell death. An additional ultrastructural finding shows that the reticulocytes anchored to the central macrophages are transported into the peripheral blood circulation.

Animals↗
PubMed1992

A truncated erythropoietin receptor that fails to prevent programmed cell death of erythroid cells.

A form of the human erythropoietin receptor (EPOR) was identified in which the cytoplasmic region is truncated by alternative splicing. The truncated form of the receptor (EPOR-T) is the most prevalent form of EPOR in early-stage erythroid progenitor cells, but the full-length EPOR (EPOR-F) becomes the most prevalent form in late-stage progenitors. EPOR-T can transduce a mitogenic signal. However, cells transfected with EPOR-T are more prone to programmed cell death than those expressing EPOR-F. EPOR-F may transduce a signal to prevent programmed cell death that is independent of the mitogenic signal, and alternative splicing of the EPOR gene may have an important role in erythropoiesis.

Amino Acid Sequence↗
PubMed2005

Podocalyxin is a CD34-related marker of murine hematopoietic stem cells and embryonic erythroid cells.

Podocalyxin/podocalyxin-like protein 1 [PCLP1]/thrombomucin/MEP21 is a CD34-related sialomucin. We have performed a detailed analysis of its expression during murine development and assessed its utility as a marker of hematopoietic stem cells (HSCs) and their more differentiated progeny. We find that podocalyxin is highly expressed by the first primitive hematopoietic progenitors and nucleated red blood cells to form in the embryonic yolk sac. Likewise, podocalyxin is expressed by definitive multilineage hematopoietic progenitors and erythroid precursors in fetal liver. The level of podocalyxin expression gradually declines with further embryo maturation and reaches near-background levels at birth. This is followed by a postnatal burst of expression that correlates with the seeding of new hematopoietic progenitors to the spleen and bone marrow. Shortly thereafter, podocalyxin expression gradually declines, and by 4 weeks postpartum it is restricted to a rare population of Sca-1(+), c-kit(+), lineage marker(-) (Lin(-)) cells in the bone marrow. These rare podocalyxin-expressing cells are capable of serially reconstituting myeloid and lymphoid lineages in lethally irradiated recipients, suggesting they have HSC activity. In summary, we find that podocalyxin is a marker of embryonic HSCs and erythroid cells and of adult HSCs and that it may be a valuable marker for the purification of these cells for transplantation.

Animals↗
PubMed1995

Emergence of myeloid cells from cultures of J2E erythroid cells is linked with karyotypic abnormalities.

J2E cells are an erythroid cell line immortalized at the proerythroblast stage of differentiation by the J2 retrovirus which contains the raf and myc oncogenes. In response to erythropoietin, these cells terminally differentiate into mature, hemoglobin-producing erythroid cells. We have shown previously that B cells overexpressing raf and myc acquired the phenotype of macrophages, and here we demonstrate that, under adverse growth conditions, myeloid cells can also emerge from J2E cultures. Morphologically, ultrastructurally, and by cytochemical analyses, these cells resembled monocytic precursor cells at different stages of differentiation. They no longer responded to erythropoietin, failed to express an erythroid-specific surface antigen, and ceased producing transcripts for globin genes, GATA-1 and SCL. Most of the converted cells displayed surface antigens typically found on myeloid cells and in vivo produced histiocytomas with severe cachexia, instead of erythroleukemias. All of the myeloid convertants had karyotypic abnormalities, and we speculate that these mutations may have triggered the transition from erythroid to myeloid phenotype. Overexpression of raf and myc oncogenes may have generated genetic instability, which then influenced the commitment of cells to specific lineages.

Animals↗
PubMed1984

Monoclonal antibodies detecting antigenic determinants with restricted expression on erythroid cells: from the erythroid committed progenitor level to the mature erythroblast.

Two new cell surface antigens specific for the erythroid lineage were defined with cytotoxic IgM monoclonal antibodies (McAb) (EP-1; EP-2) that were produced using BFU-E-derived colonies as immunogens. These two antigens are expressed on in vivo and in vitro derived adult and fetal erythroblasts, but not on erythrocytes. They are not detectable on resting lymphocytes, concanavalin-A (Con-A) activated lymphoblasts, granulocytes, and monocytes or granulocytic cells or macrophages present in peripheral blood or harvested from CFU-GM cultures. Cell line and tissue distributions distinguish McAb EP-1 and EP-2 from all previously described monoclonal antibodies. McAb EP-1 (for erythropoietic antigen-1) inhibits the formation of BFU-E and CFU-E, but not CFU-GM, colonies in complement-dependent cytotoxicity assays. By cell sorting analysis, about 90% of erythroid progenitors (CFU-E, BFU-E) were recovered in the antigen-positive fraction. Seven percent of the cells in this fraction were progenitors (versus 0.1% in the negative fraction). The expression of EP-1 antigen is greatly enhanced in K562 cells, using inducers of hemoglobin synthesis. McAb EP-2 fails to inhibit BFU-E and CFU-E colony formation in complement-dependent cytotoxicity assays. EP-2 antigen is predominantly expressed on in vitro derived immature erythroblasts, and it is weakly expressed on mature erythroblasts. The findings with McAb EP-1 provide evidence that erythroid progenitors (BFU-E and CFU-E) express determinants that fail to be expressed on other progenitor cells and hence appear to be unique to the erythroid lineage. McAb EP-1 and EP-2 are potentially useful for studies of erythroid differentiation and progenitor cell isolation.

Animals↗
PubMed1976

The absence of cell-specific histone in erythroid cell from rabbit marrow.

The histone complements of erythroid cells from anemic rabbit marrow and cell fractions enriched in orthochromatic erythroblasts were examined using a variety of techniques. None of these methods revealed the presence of a histone comparable to H5, the erythrocyte-specific histone of birds and fish. Purified histones H1, H2A, H2B, H3 and H4 from rabbit marrow nuclei showed no unusual amino acid compositions.

Amino Acids↗
PubMed2000

Generation and characterization of a neutralizing monoclonal antibody against erythroid cell stimulating factor.

Erythroid cell stimulating factor (ESF) is present in mouse serum and has been reported to function in concert with erythropoietin (EPO) in the formation of erythroid cells in in vitro culture systems. We report here the generation and characterization of a monoclonal antibody (MAb) directed against ESF, with potent anti-ESF-neutralizing activity. A hybridoma-producing MAb to ESF was selected following enzyme-linked immunosorbent assay (ELISA)-based screening of 270 colonies obtained from a fusion of immunized mouse splenocytes with NS1 myeloma cells. Western blot analyses of mouse serum using this antibody specifically detected a single protein (approximate molecular weight of 60 kDa and 120 kDa, under reducing and nonreducing conditions, respectively) corresponding to ESF, with no reactivity to EPO. Furthermore, this MAb demonstrated reactivity to a protein similar in molecular mass, across species, showing reactivity in sera obtained from human, horse, goat, guinea pig, rabbit, and rat. Immuno-chemical characterization demonstrated this antibody to be of IgG3 isotype, bearing kappa light chains. Injection of this monoclonal anti-ESF antibody to exhypoxic polycythemic mice at 6 and 24 h after EPO injection significantly reduced 59Fe incorporation into red blood cells, demonstrating its ability to neutralize in vivo erythropoiesis in our mouse model system. Thus, this novel erythroid cell-specific MAb will be an invaluable tool for further delineating the physiological role of ESF in in vivo erythropoiesis.

Animals↗
PubMed2003

The regulatory effect of heme on erythroid aminolevulinate synthase in natural erythroid cells.

A major enzymatic pathway in erythroid cells is the eight-step formation of heme, starting with the erythroid isoform of aminolevulinate synthase (eALAS). We studied the regulation of eALAS synthesis by heme in natural erythroid cells. Erythroid cells from mouse blood or bone marrow were incubated with different concentrations of heme and labelled with [35S]methionine. This was followed by immunoprecipitation of eALAS proteins. Northern blot analysis was done on mRNA isolated from bone marrow. Incubation with heme (5-100 muM) was shown to clearly inhibit eALAS synthesis in erythroid cells of bone marrow. This inhibitory effect of heme could also be observed in peripheral blood cells at higher concentrations while the preform of eALAS was rather increased. However, at lower concentrations of heme (1-10 microM), eALAS synthesis increased. Northern blot studies argued the inhibitory effect was at the posttranscriptional level. Our results suggest that the net effect of murine eALAS regulation by heme varies with the degree of erythroid differentiation. Heme formation seems to be more tightly controlled in the bone marrow (nucleated) cells in order to prevent oxidative cell damage, compared to more differentiated erythroid cells.

5-Aminolevulinate Synthetase↗
PubMed1976

Erythroid cell differentiation.

We have reviewed erythroid cell differentiation from two points of view: 1) differences between fetal and adult human red cells with particular reference to alterations which can occur in the normal pattern of erythroid cell development during the course of leukemia; 2) beochemical events which occur during erythroid cell maturation, as a model system for the study of the control of gene expression. During the course of many leukemias there is the synthesis of red cells containing fetal hemoglobin. In most cases this phenomenon is limited to a small population or clone of red cells and probably represents a nonspecific response of the bone marrow to a hematologic stress. However, in juvenile chronic myeloid leukemia and, in rare cases of erythroleukemia, there is a major reversion to fetal erythropoiesis, with progressive increase in fetal hemoglobin levels and synthesis of red cells which contain not only fetal hemoglobin but have a true fetal pattern of protein synthesis affecting proteins other than Hb F, namely Hb A2, carbonic anhydrase and the membrane antigens i and I. In this case, the fetal erythropoiesis may be a more specific manifestation of the leukemic process and may be related to the phenomenon of fetal protein synthesis (alpha-fetoprotein of carcinoembryonic antigen) observed in other types of neoplasia. Further information on the etiology and pathogenesis of abnormal cell proliferation and differentiation in the leukemias can be obtained by the study of experimental systems permitting the investigation of the regulation of gene expression in differentiating mammalian cells. Maturing erythroid cells provide a promising system for such investigations for many reasons: differentiating erythroid cells can be obtained relatively free of other cell types; a large amount of a well characterized product, hemoglobin, is synthesized; techniques are now available that permit isolation of erythroid precursors at different stages of differentiation (5-8); and finally, highly sensitive methods of measuring globin mRNA levels by DNA-RNA hybridization are currently available (13, 26, 27). We have used such techniques to measure levels of globin mRNA in separated populations of murine erythroid cells at different stages of maturation. These studies demonstrated a correlation between globin mRNA content and degree of morphological maturation. In the least well differentiated cells, however, there appeared to be a disproportionate amount of mRNA for the level of hemoglobin synthesis in these cells. These results suggest the presence of some translational control of globin mRNA in the early stages of erythroid development, although the major control of globin gene expression in this system seems to be at the transcriptional level...

Anemia, Hemolytic↗
PubMed1991

Species-nonspecific action of soluble immunosuppressive factor produced by murine immature erythroid cells.

Immature murine erythroid cells have natural suppressor cell activity suppressing in vitro mouse plaque-forming cell response and LPS-stimulated proliferative response of mouse spleen cells. A cell population enriched by erythroid precursors can produce a soluble activity with similar suppressive abilities. This erythroid suppressor activity (ErSF) has a low Mr (1 to 10 kDa). It can suppress both IgM and IgG secretion of PWM-stimulated human B cells and inhibit the proliferative response of PWM-stimulated human B lymphocytes, thereby indicating a species-nonspecific type of action. Antigen-induced mouse PFC response and mitogen-stimulated mouse and human B cell proliferation were inhibited dose dependently by the addition of ErSF, which did not significantly reduce cell viability, however. Kinetic studies showed that ErSF suppressed Ig secretion and proliferation of mitogen-stimulated B lymphocytes in all culture periods. The suppressive effect of ErSF on B cell proliferation was indirect, requiring the presence of IL-2 (but not of IL-1 alpha, IL-1 beta, or BCGF). In the presence of IL-2, the proliferative response of SAC-stimulated B cells was suppressed by ErSF when added at all time intervals studied but was maximal when ErSF was added on the third day of culture. The role of suppressor factor produced by immature murine erythroid cells in the phenomenon of "natural suppression" has been discussed.

Animals↗
PubMed1975

Use of cell separation and short-term culture techniques to study erythroid cell development.

Cell populations highly enriched for the different stages of erythroid cell maturation were obtained by three sequential operations: harvesting of erythroid cells after induction of erythroid hyperplasia in the spleens of mice, elimination of the more mature erythrocytes by immunologic techniques, and separation of the residual nucleated erythroid cells as a function of size by the velocity sedimentation technique. The resulting cell fractions were studied both directly and after overnight incubation in the presence or absence of erythropoietin. In short-term culture, erythropoietin stimulated proliferation of pronormoblasts and basophilic normoblasts but probably not cells at later stages of differentiation. Erythropoietin also appeared to recruit increased numbers of pronormoblasts. In this experimental system, erythroid cell differentiation was able to proceed in the absence of erythropoietin, but without proliferation of these early erythroid cells. These techniques have provided a model system for the study of erythroid cells at different stages of maturation isolated from a uniform source at one point in time. The morphologic observations indicated that erythropoietin stimulates erythroid cell proliferation at several early stages of the maturation pathway.

Anemia, Hemolytic↗
PubMed1998

The apoptotic and nonapoptotic nature of the terminal differentiation of erythroid cells.

The morphology of erythroid cells changes dramatically during the course of their terminal differentiation. According to calculations made with cytospin preparations obtained from Syrian hamster yolk-sac-derived erythroid cells, the area of nuclei at day 10 of gestation ranges from 25 to 85 micron 2 and is reduced to 15-25 micron 2 on day 13 [K. Morioka and R. Minamikawa-Tachino, Dev. Growth Differ. 35, 569-582, 1993]. The DNA and protein contents of each nucleus also decrease during this period. Nonspecific fragmentation of DNA was detected by agarose gel electrophoresis in all samples obtained from day 10 to day 13 of gestation, while distinct ladders of DNA fragments were not detected. DNA fragmentation was also detected by an in situ DNA-end labeling (TUNEL) assay. As the terminal differentiation proceeded, gradual decreases in levels of both histone H1 and most nonhistone proteins were observed by SDS-polyacrylamide gel electrophoresis, while levels of core histones appeared to be constant. In particular, lamin B2 was almost completely lost from the nuclear matrix fraction on day 11. These results suggest that the terminal differentiation of erythroid cells and apoptosis might have common mechanisms. However, expansion of the cytoplasm during the terminal differentiation distinguishes these processes. In addition, in the erythroid terminal differentiation, nuclei never form lobules or become fragmented; no apoptotic bodies are formed, occurrence of the apoptosis-like cellular change is not sporadic but rather synchronous, and the process is slow, with at least several days being required for cell death. These characteristics are different from those of typical apoptosis. Thus, the terminal differentiation of nucleated embryonic erythroid cells exhibits both apoptotic and nonapoptotic features.

Animals↗