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PubMed2006

Suppression of erythropoiesis in malarial anemia is associated with hemozoin in vitro and in vivo.

Malarial anemia is a global public health problem and is characterized by a low reticulocyte response in the presence of life-threatening hemolysis. Although cytokines, in particular tumor necrosis factor-alpha (TNF-alpha), can suppress erythropoiesis, the grossly abnormal bone marrow morphology indicates that other factors may contribute to ineffective erythropoiesis. We hypothesized that the cytotoxic hemozoin (Hz) residues from digested hemoglobin (Hb) significantly contribute to abnormal erythropoiesis. Here, we show that not only isolated Hz, but also delipidated Hz, inhibits erythroid development in vitro in the absence of TNF-alpha. However, when added to cultures, TNF-alpha synergizes with Hz to inhibit erythropoiesis. Furthermore, we show that, in children with malarial anemia, the proportion of circulating monocytes containing Hz is associated with anemia (P < .001) and reticulocyte suppression (P = .009), and that this is independent of the level of circulating cytokines, including TNF-alpha. Plasma Hz is also associated with anemia (P < .001) and reticulocyte suppression (P = .02). Finally, histologic examination of the bone marrow of children who have died from malaria shows that pigmented erythroid and myeloid precursors are associated with the degree of abnormal erythroid development. Taken together, these observations provide compelling evidence for inhibition of erythropoiesis by Hz.

Anemia↗

PubMed2006

STAT5 acts as a repressor to regulate early embryonic erythropoiesis.

STAT5 regulates definitive (adult stage) erythropoiesis through its ability to transduce signals from the erythropoietin receptor. A function for STAT-dependent signaling during primitive (embryonic) erythropoiesis has not been analyzed. We tested this in the Xenopus system, because STAT5 is expressed at the right time and place to regulate development of the embryonic primitive ventral blood island. Depletion of STAT5 activity results in delayed accumulation of the first globin-expressing cells, indicating that the gene does regulate primitive erythropoiesis. Our results suggest that in this context STAT5 functions as a repressor, since forced expression of an activator isoform blocks erythropoiesis, while embryos expressing a repressor isoform develop normally. The erythroid phenotype caused by the activator isoform of STAT5 resembles that caused by overexpression of fibroblast growth factor (FGF). We show that STAT5 isoforms can function epistatic to FGF and can be phosphorylated in response to hyperactivated FGF signaling in Xenopus embryos. Therefore, our data indicate that STAT5 functions in both primitive and definitive erythropoiesis, but by different mechanisms.

Animals↗

PubMed1975

Erythropoiesis and erythropoietin in hypo- and hyperthyroidism.

Qualitative and quantitative studies of erythropoiesis in 23 patients with hypothyroidism and 21 patients with hyperthryoidism included routine hematologic evaluation, bone marrow morphology, status of serum iron, B12 and folate red blood cell mass and plasma volume by radioisotope methods, erythrokinetics and radiobioassay of plasma erythropoietin. A majority of patients with the hypothyroid state had significant reduction in red blood cell mas per kg of body weight. The presence of anemia in many of these patients was not evident from hemoglobin and hematocrit values due to concomitant reduction of plasma volume. The erythrokinetic data in hypothyroid patients provided evidence of significant decline of the erythropoietic activity of the bone marrow. Erythroid cells in the marrow were depleted and also showed reduced proliferative activity as indicated by lower 3H-thymidine labeling index. Plasma erythropoietin levels were reduced, often being immeasurable by the polycythemic mouse bioassay technique. These changes in erythropoiesis in the hypothyroid state appear to be a part of physiological adjustment to the reduced oxygen requirement of the tissues due to diminished basal metabolic rate. Similar investigations revealed mild erythrocytosis in a significant proportion of patients with hyperthyroidism. Failure of erythrocytosis to occur in other patients of this group was associated with impaired erythropoiesis due to a deficiency of hemopoietic nutrients such as iron, vitamin B12 and folate. The mean plasma erythropoietin level of these patients was significantly elevated; in 4 patients the levels were in the upper normal range whereas in the rest, the values were above the normal range. The bone marrow showed erythyroid hyperplasia in all patients with hyperthyroidism. The mean 3H-thymidine labeling index of the erythroblasts was also significantly higher than normal in hyperthyroidism; in 8 patients the index was within the normal range whereas in the remaining 13 it was above the normal range. Erythrokinetic studies also provided evidences of increased erythropoietic activity in the bone marrow. It is postulated that thyroid hormones stimulate erythropoiesis, sometimes leading to erythrocytosis provided there is no deficiency of hemopoietic nutrients. Stimulation of erythropoiesis by thryoid hormones appears to be mediated through erythropoietin.

Biological Assay↗

PubMed2006

Hepcidin mRNA levels in mouse liver respond to inhibition of erythropoiesis.

Hepcidin, a key regulator of iron metabolism, decreases intestinal absorption of iron and its release from macrophages. Iron, anemia, hypoxia, and inflammation were reported to influence hepcidin expression. To investigate regulation of the expression of hepcidin and other iron-related genes, we manipulated erythropoietic activity in mice. Erythropoiesis was inhibited by irradiation or posttransfusion polycythemia and stimulated by phenylhydrazine administration and erythropoietin. Gene expression of hepcidin and other iron-related genes (hemojuvelin, DMT1, ferroportin, transferrin receptors, ferritin) in the liver was measured by the real-time polymerase chain reaction. Hepcidin expression increased despite severe anemia when hematopoiesis was inhibited by irradiation. Suppression of erythropoiesis by posttransfusion polycythemia or irradiation also increased hepcidin mRNA levels. Compensated hemolysis induced by repeated phenylhydrazine administration did not change hepcidin expression. The decrease caused by exogenous erythropoeitin was blocked by postirradiation bone marrow suppression. The hemolysis and anemia decrease hepcidin expression only when erythropoiesis is functional; on the other hand, if erythropoiesis is blocked, even severe anemia does not lead to a decrease of hepcidin expression, which is indeed increased. We propose that hepcidin is exclusively sensitive to iron utilization for erythropoiesis and hepatocyte iron balance, and these changes are not sensed by other genes involved in the control of iron metabolism in the liver.

Anemia, Hemolytic↗

PubMedDate not supplied

Effects of human recombinant erythropoietin on differentiation and distribution of erythroid progenitor cells on murine medullary and splenic erythropoiesis during hypoxia and post-hypoxia.

Hemopoietic cells, the extracellular matrix, growth factors and the microenvironment are involved in the regulation of hemopoiesis. Although the regulation of erythropoiesis is well understood at the cellular level in vivo and in vitro, the role of hemopoietic sites of erythroid progenitors production has not been well defined in both steady state conditions and in stress erythropoiesis. In this study we examined the qualitative erythroid differentiation and quantitative changes of the erythroid progenitors in different erythropoietic organs during erythropoiesis of stress in a hypoxia-induced polycythemia and post-hypoxic changes in a mice model. Chronic intermittent exposure to hypobaric hypoxia induced polycythemia in mice and the post-hypoxic period was characterized by total suppression of erythropoiesis. The number and distribution in hemopoietic sites of Immature Erythroid Burst (BFU-EI), Mature Erythroid Burst (BFU-EM) and Erythroid Colony Forming Units (CFU-E) was evaluated in bone marrow and spleen of hypoxic and post-hypoxic mice after removal from the chamber. The number of BFU-EI and CFU-E, was evaluated in both femoral bone marrow and spleen of ex-hypoxic polycythemic mice, at two times intervals after the end of hypoxia. We found that in both bone marrow and spleen, the kinetics of the CFU-E pool was characterized by a sharp fall from above normal to lower than normal levels. BFU-EM increased from normal to higher than normal levels. These results have been correlated with both erythropoietin (EPO) and the erythropoietic activity. The results show that EPO levels largely control both the differentiation and the amplification of the CFU-E pool and they suggest that EPO may acts as a "survival factor" at the CFU-E level and/or increase the flow of cells from BFU-E to CFU-E. After the termination of the period of hypoxia and during post-hypoxia there was a reduction in EPO production which subsequently caused a depletion of the CFU-E population, indicating that the size of the CFU-E pool is EPO-dependent. After the injection of 1U of recombinant human erythropoietin (rHuEPO) the size of that pool was increased and the pool of BFU-EI was decreased. It is noteworthy that our studies show that the spleen functions as a large reservoir of erythroid precursors for hypoxia-induced stress erythropoiesis.

Animals↗

PubMed1992

Long-term recombinant human granulocyte colony-stimulating factor (rhG-CSF) treatment severely depresses murine marrow erythropoiesis without causing an anemia.

We hereby report profound effects of long-term granulocyte colony-stimulating factor (G-CSF) administration on murine erythropoiesis. Recombinant human (rh)G-CSF (150 micrograms/kg body weight/day) was administered over 24 days to female C57Bl mice. Marrow erythroid colony-forming units (CFU-E) and erythroblast numbers declined to less than 5% of normal, whereas splenic erythropoiesis simultaneously increased. Splenic erythropoiesis effectively compensated for the loss of marrow erythropoiesis as indicated by the maintenance of a normal hematocrit. In the marrow the numbers of spleen colony-forming units (CFU-S) and erythroid burst-forming units (BFU-E) declined as well. Simultaneously, however, these numbers increased both in the spleen and in the peripheral blood by a factor of 20 to 30. These findings suggest a continuous migration of stem cells and progenitor cells out of the marrow and an efficient seeding in the spleen, directly or indirectly induced by G-CSF. In addition the differentiation and/or amplification of BFU-E to CFU-E was impaired in the marrow but not in the spleen. The marrow and splenic microenvironment also behaved differently with respect to granulopoiesis. G-CSF did not lead to an enhanced granuloid amplification in the spleen but exerted its proliferation activity mainly in the marrow. These findings imply that prolonged G-CSF treatment might cause erythroid depression in animals and humans when spleen erythropoiesis is less efficient than in mice.

Anemia↗

PubMed2005

[The effects of burn serum on the erythropoiesis and granulopoiesis in bone marrow in mice].

OBJECTIVE: To observe the effects of burn serum on the erythropoiesis and granulopoiesis in bone marrow in mice, and to explore the possible underlying mechanism. METHODS: Murine bone marrow cell (BMC) strain was prepared routinely and was employed in the establishment of the culture system of colony forming units of erythrocytes, or granulocytes and monocytes. To both sets of culture system normal murine serum (N group) and burn serum, which was collected from the mice with 15% full thickness burn at 12 postburn hours (PBH) and 1, 3, 5, 7 and 10 postburn days (PBD), (burn serum group) was added. In addition, positive control and blank control groups were set accordingly. The stimulating activity of all kinds of sera on the BMCs in the two sets of culture system was determined. The changes in the burn serum concentrations of EPO and GM-CSF were detected by radioimmunoassay, and the data were analyzed by logarithmic linear fitting correlation with the former influence of burn sera on the erythrocytes and granulocytes. RESULTS: (1) Burn sera exhibited obvious stimulation promoting activity on the erythropoiesis and granulopoiesis in BMC, and the activity peaked (384 +/- 60 and 127 +/- 16 CFU) on 1 PBD and decreased thereafter to approach the values found in normal sera group (125 +/- 14 and 34 +/- 20 CFU) on 7 PBD. (2) The EPO content in burn serum was evidently higher than the normal value (P < 0.01) during 12 PBH to 7PBD period. The GM-CSF concentration was obviously higher than the normal value (P < 0.05) at 12 PBH and on 1 PBD. (3) The EPO concentration in burn serum was significantly and logarithmically correlated with the stimulation promoting activity of burn serum on erythropoiesis (r = 0.8570, P = 0.0137). But the GM-CSF concentration in culture with burn serum was not correlated with the stimulation promoting activity of burn serum on granulopoiesis (r = 0.7049, P > 0.05). CONCLUSION: The sera harvested from burned mice during early postburn stage exhibited strong stimulation promoting activity on the erythropoiesis and granulopoiesis in bone marrow. The increased EPO level in burn serum might be the important factor contributing strong stimulation action on erythropoiesis, while increased GM-CSF level was not.

Animals↗

PubMed1991

Erythropoietin levels and inhibition of erythropoiesis in end-stage renal failure.

Anaemia of chronic renal failure is multifactorial. Twenty-one patients with end-stage renal disease (ESRD) and 21 normal subjects were studied to determine the significance of serum erythropoietin levels and erythropoiesis inhibition in the aetiology of renal anaemia. Serum erythropoietin levels and erythropoiesis inhibition were measured by determining the incorporation of labelled-thymidine into the DNA of rabbit bone marrow cells. The mean haemoglobin concentration was 9.0 +/- 0.5 g/dl (mean +/- SEM) in ESRD and 14.4 +/- 0.4 g/dl in normal controls. Serum erythropoietin levels (99.9 +/- 17.9 mU/ml in ESRD vs 74.9 +/- 9.7 mU/ml in normal controls) and inhibition of erythropoiesis (252 +/- 28.9 in ESRD vs 186.2 +/- 19.4 in normal controls) were not significantly different in both groups. However, erythropoiesis inhibition had a significant correlation with the degree of anaemia (p less than 0.01). The results suggest that erythropoiesis inhibition play a significant role in the pathogenesis of renal anaemia.

Adult↗

PubMed1990

Modulation of erythropoiesis and myelopoiesis by exogenous erythropoietin in human long-term marrow cultures.

In spite of their ability to support myelopoiesis for several months, human long-term marrow cultures (LTMC) are unable to sustain the production of mature erythroid cells for greater than 4 weeks. Because this preference correlates with the presence of myeloid growth factors and possible absence of erythroid factors in LTMC, we studied the effects of the erythroid growth and differentiation factor erythropoietin (Epo) on both erythropoiesis and myelopoiesis in human LTMC. Either natural or recombinant Epo was added weekly to LTMC for 10 weeks, and total cell number, numbers of hemopoietic progenitors (mixed lineage colony-forming units, CFU-MIX; erythroid burst-forming units, BFU-E; erythroid CFU, CFU-E; granulocyte-macrophage CFU (CFU-GM); granulocyte CFU, CFU-G; and macrophage CFU, CFU-M), erythroblasts (early and late), granulocytes, and macrophages were quantitated separately in the adherent and nonadherent layers of the cultures. In the absence of Epo, mature erythroid cells disappeared within the first 3-4 weeks, whereas in cultures supplemented with Epo, erythropoiesis was supported for up to 8 weeks. Results indicate that erythroid maturation is blocked at the BFU-E stage and that exogenous Epo may act on a mature subpopulation of BFU-E located in the nonadherent fraction of the cultures, promoting its maturation into CFU-E, which in turn develop into erythroblasts. However, despite Epo supplementation, erythropoiesis was not restored to in vivo proportions, suggesting that additional factors or conditions necessary for erythropoiesis are lacking in LTMC. Interestingly, we found that exogenous Epo reduced the numbers of presumably more mature (nonadherent) myeloid CFU (CFU-C), granulocytes, and macrophages compared to controls and did not alter the levels of any of the most primitive hemopoietic progenitors measured (CFU-MIX, adherent BFU-E, and adherent CFU-C). Thus the data show that exogenous Epo modulates hemopoiesis in human LTMC, enhancing erythropoiesis and suppressing myelopoiesis, but that its effects appear limited to modulating levels of the nonadherent (more mature) progenitors, leaving the numbers of the adherent (immature) progenitor cells unchanged.

Bone Marrow Cells↗

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↗

PubMed1985

[Interrelation of erythropoiesis and lymphopoiesis in experimental infectious processes and in viral leukemogenesis].

Interrelation of erythropoiesis and immune response was studied in mice of various lines infected with mycoplasma species, Shigella flexneri 2a and Rauscher leukemia virus (R-MLV). Intensity of erythropoiesis was estimated by the endocolonization data of sublethally irradiated mice and 59Fe incorporation, while immune reactivity--by generation of splenic antibody-forming cells in response to immunization with sheep erythrocytes. The inverse correlation between the ability of infectious agents to enhance erythropoiesis and to depress immune reactivity was found. Enhanced state of erythropoiesis was observed with concomitant diminished immune response when R-MLV and M. arthritidis or S. flexneri 2a (strain 516) were used. There was a positive correlation between the ability of mycoplasmae and shigellae to activate erythropoiesis and their stimulatory effect on R-MLV reproduction tested by the spleen focus-forming units (SFFU) enumeration technique. Possible role of mononuclear phagocytes in the phenomena mentioned is discussed.

Animals↗

PubMed1985

Further studies on cyclic erythropoiesis in mice.

When young adult female W/Wv mice are given 0.5 micro+Ci 89Sr/g body weight intravenously, their hematocrit values oscillate from nadirs of 26% to zeniths of 42% with a periodicity of 16 days [1]. The response of the W/Wv mouse to an assortment of radioactive and hematologic stresses have been examined in an effort to understand better the pathophysiology of cyclic erythropoiesis. When the dose of 89Sr is increased, the amplitude of cycling increases as nadirs are lowered, but periodicity is unchanged. When the dose of 89Sr is lowered to 0.3 microCi or less, cyclic erythropoiesis of substantial amplitude is observed only after five or six microoscillations. A single hematopoietic insult of 80 rad x-irradiation coupled with phlebotomy produces a transient form of cyclic erythropoiesis, namely, a series of dampened oscillations prior to recovery. Finally, we report that Wv/Wv mice exhibit a form of cyclic erythropoiesis in response to 0.5 microCi 89Sr/g body weight, in which the hematocrit values of successive nadirs gradually increase, and stabilize at about 100 days. 89Sr does not induce cyclic erythropoiesis in the +/+, W/+, or W/v/+ mice, the Hertwig strain of anemic mice, or in normal BDF1 mice.

Anemia↗

PubMed1982

The distribution of erythropoiesis over the various anatomical regions of the erythropoietic system in some inbred strains of mice.

The extraction of 59Fe bound to the heme in the erythropoietic organs by means of acid ethylacetate was used to establish the proportion of erythropoiesis for which individual bones and the spleens of some inbred mouse strains are responsible. The proportion of splenic erythropoiesis differs from strain to strain, being in the range 9-42% of total erythropoiesis. In the strain BALB/c erythropoiesis is shifted in comparison with C57B1/10 strain towards the spine and away from the bones of the skull, the long bones of the limbs and the pelvis. Calculations of the erythroid cellularity and/or the intensity of erythropoiesis of the total bone marrow on the basis of a single bone should take into account both these interstrain differences in the participation of different regions and the possibility of various proportions of red and white blood cells and cells containing non-heme iron existing in different regions (bones).

Animals↗

PubMed1980

beta 2-Adrenergic stimulation of erythropoiesis in busulfan treated mice.

The capability of chronic beta 2-adrenoceptor activation to effectively stimulate erythrocyte production in vivo was investigated in mice which had been treated with the hematopoiesis inhibiting agent busulfan. A relatively low dose (5 mg/kg i.p.) of busulfan produced moderate depression of erythropoiesis 10 days after a single injection, as determined by 59Fe-incorporation into erythrocytes. Administration of albuterol (1 mg/kg s.c. twice daily), a selective beta 2-adrenergic agonist, significantly enhanced erythropoiesis for 5--10 days after the injection of busulfan. In a long-term study with albuterol at the same dose a significant increase in hematocrit values as well as in the circulating erythrocyte mass was found in busulfan (5 mg/kg i.p. weekly) treated mice when compared to saline-busulfan treated control mice. Simultaneous injections of the beta-adrenergic blocking agent propanolol (4 mg/kg i.p.) diminished the effect of albuterol on erythropoiesis. Albuterol at a lower dose (0.1 mg/kg) had no significant effect on erythrocyte mass. In view of recent findings, which have shown that the proliferation of the pluripotent hemopoietic stem cell pool is blocked by busulfan, it is concluded that the main site of beta 2-adrenergic action on erythropoiesis is on the erythroid committed stem cell pool. In addition, enhanced release of erythropoietin from the kidney following the application of albuterol may contribute to beta 2-adrenergic stimulation of erythropoiesis.

Albuterol↗

PubMed1980

Cancer cell inhibition of erythropoiesis.

In this study we have used tissue culture techniques to explore the mechanism by which metastatic cancer cells in the bone marrow interfere with erythropoiesis. The effect of transplantable Walker-256 (W256) cancer cells on Ep-stimulated erythroid colony formation (CFU-E) in methylcellulose cultures and 59Fe-heme synthesis by rat marrow cells in suspension cultures was studied. The number of CFU-Es per 4 X 10(5) marrow cells decreased by 55% in the presence of 4 X 10(2) cancer cells. Likewise, the stimulatory effect of Ep on normal marrow heme synthesis decreased by 89% when cancer cells were added to marrow cell cultures. By the immobilization of the cancer cells in an agar underlayer, the inhibitory effect of cancer cells on marrow erythropoiesis in an upper methylcellulose layer was demonstrated to be independent of cell contact. The CFU-E growth-inhibitory effect of cancer cells could be attenuated by drugs which interfere with cancer cell protein and DNA synthesis. Although these experiments suggest that cancer cells produce an inhibitor of erythropoiesis, a stable inhibitory factor was not isolated. In similar experiments, rat peritoneal macrophages were also able to inhibit in vitro erythropoiesis. We conclude that cancer cells have the capacity to inhibit erythropoiesis by a mechanism which is independent of cell contact.

Animals↗

PubMed1976

Delayed erythropoiesis in irradiated rats grafted with syngeneic marrow: effects of cytotoxic drugs and iron-deficiency anemia.

Erythropoiesis in spleens of lethally irradiated Lewis rats grafted with 4-35 X 10(6) syngeneic marrow cells was inhibited or delayed during the test period of 5 days; this was in marked contrast to observation in irradiated mice. The mechanism of this inhibition was the subject of this study. Pretreatment of recipients 9 days prior to irradiation with the cytotoxic drugs cyclophosphamide (CY), busulfan (BUS), or dimethylmyleran (DMM), or the induction of iron deficiency with anemia in recipients reversed this delayed erythropoiesis. However, neither iron-deficiency anemia nor pretreatment with BUS or DMM affected the ability of irradiated recipients to reject 20 to 50 X 10(6) allogeneic marrow cells. The administration of commercial preparations of erythropoietin to hosts stimulated erythropoiesis moderately. However, proliferation of syngeneic marrow cells was not enhanced when infused into lethally irradiated Spontaneous Hypertensive (SH) inbred-strain rats which have high levels of endogenous erythropoietin. Finally, plasma from irradiated rats treated with phenylhydrazine to produce severe anemia was rich in erythropoietin but failed to stimulate erythropoiesis in the cell transfer system. Two hypotheses are considered: (1) Irradiation inhibits the secretion of a factor (not erythropoietin) responsible for initiating early stages in differentiation of transplanted stem cells; iron-deficiency anemia and cytotoxic drugs stimulate the secretion of this factor. (2) Normal rats secrete a factor which suppresses erythropoiesis; iron-deficiency anemia and cytotoxic drugs inhibit the production or function of this factor. Cellular rather than humoral factors may by involved.

Anemia, Hypochromic↗

PubMed2004

Erythropoiesis from adult but not fetal blood-derived CD133+ stem cells depends strongly on interleukin-3.

We have shown previously that erythropoiesis in cultures from fetal blood depends less on interleukin-3 (IL3) than erythropoiesis from adult blood. This paper explores if this is due to different proportions of stem cell sub-populations with different IL3 requirement, or to different IL3 requirement on fetal and adult stem cells in general. The CD133 (AC133) antigen is found on half of all CD34+ cells with erythropoietic potential and is thought to mark a primitive stem cell sub-population. This work compares the IL3 requirements of CD133+ and CD133-CD34+ cells derived from fetal (12-20 weeks) and adult blood. Erythropoiesis was monitored using flow cytometry and colony counting. Erythropoiesis from adult CD133+ but not CD133-CD34+ cells was dramatically delayed (6-8 days) in the absence of IL3. In cultures from fetal blood, both CD133+ and CD133-CD34+ cells showed only a small dependency on IL3. The ratio of erythroid colony-forming CD133+ cells to erythroid colony-forming CD34+ cells was 0.5-0.6 in adult and 0.2-0.4 in fetal blood. The differential IL3 dependency of erythropoiesis from fetal and adult blood CD133+ and CD133-CD34+ stem cells may be relevant for the choice and preparation of stem cells for clinical purposes.

AC133 Antigen↗

PubMed1978

[Erythropoietin and erythropoiesis inhibitor in neonatal hypoxia and normal conditions].

In 22 healthy newborns and in 31 newborns with transposition of the major arterial vessels (TMAV) erythropoietin and erythropoiesis inhibitor was studied on a model of polycythemic mice. Erythropoietin was not detected, whereas erythropoiesis inhibitor was revealed in the plasma and urine of 5--7-day-old healthy newborns. The newborns with TMAV displayed a rise of erythropoietin level up to the 14th day and its reduction during the period of from 14th to the 56th days. Erythropoiesis inhibitor was also found in the urine concentrates of the newborn with TMAV during the period of 3--4 weeks. The role of erythropoiesis inhibitor as a physiological regulator appearing in the blood of healthy and hypoxic newborns to normalize the erythropoiesis in the course of the initial weeks after birth is discussed.

Erythropoietin↗