Regulation of Erythropoiesis. Xx. Kinetics of Red Cell Production*

Stohlman, Frederick; Ebbe, Shirley; Morse, Bernard S.; Howard, Donald; Donovan, Janet

doi:10.1111/j.1749-6632.1968.tb15149.x

Cited by 89 publications

(30 citation statements)

References 25 publications

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“…It is therefore possible that the slight elevation of HbF in peripheral blood of pregnant women is the reflection of stimulated erythropoiesis and release of erythroid cells at earlier maturational stages (28). Similar mechanisms may be in operation to account for the increased level of HbF observed in a number of pathological conditions such as leukemia and aplastic anemia.…”

Section: Methodsmentioning

confidence: 95%

Proportion of fetal hemoglobin synthesis decreases during erythroid cell maturation.

Chui¹,

Wong²,

Enkin³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

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Peripheral blood mononuclear cells from pregnant and postpartum women were cultured in vitro with erythropoietin. Burst-forming unit (BFU-E)derived erythroid colonies composed of immature erythroblasts with low hemoglobin contents were observed by day 8 of culture. By day 12 of culture, numerous BFU-E-derived erythroid colonies with high hemoglobin contents were present. The Y/(y + f) globin synthetic ratio was approximately 12% in the early cultures and 6% in the late cultures, indicating that the proportion of fetal hemoglobin synthesis decreases during erythroid cell maturation. These studies also reveal that the capacity for fetal hemoglobin production by peripheral blood BFU-E in vitro is not altered during pregnancy.The major hemoglobin in humans during intrauterine life is fetal hemoglobin, a2Y2. Adult hemoglobin, a232, is first detected at around the 10th week of gestation and accounts for approximately 10% of all hemoglobins present until about the 30th week of gestation, when increasing amounts of adult hemoglobin are produced (1). By the time the infant is 6 months old, most of the hemoglobin present is adult hemoglobin (2). The mechanisms for the switching of hemoglobins during fetal development are presently not clear (3). These orderly ontogenetic changes provide an excellent model for studying gene regulation and expression. In addition, elucidation of the mechanisms for hemoglobin switching can provide a potentially useful approach to the therapy of patients with genetic disorders involving the j globin chain.Immature erythroid stem cells, burst-forming units that respond to erythropoietin (BFU-E), are present in adult human peripheral blood and can proliferate and differentiate into large colonies of erythroblasts in vitro (4, 5). These erythroblasts, derived from normal adult individuals, synthesize a substantial amount of fetal hemoglobin (6-8). Because HbF is increased in maternal peripheral blood during pregnancy (9-11), the present investigation was undertaken to determine if peripheral blood BFU-E in pregnant women have an increased capacity for HbF production in culture and to study the pattern of HbF synthesis during erythroid cell maturation in vitro. Evidence is presented that the capacity for HbF production by peripheral blood BFU-E in vitro is not altered during pregnancy. These studies also reveal that the proportion of HbF synthesis decreases during erythroid cell maturation. A preliminary report of these studies has been published elsewhere (12). METHODSSubjects. Forty-four pregnant and postpartum (3-7 months) women were studied. All women were healthy and had no known diseases or complications. Appropriate consent was obtained. [50][51][52][53][54][55][56][57][58][59][60] Ci/mmol; 1 Ci = 3.7 X 1010 becquerels), obtained from New England Nuclear, was added to each plasma clot on either day 6 or day 7, and either day 11 or day 12 of culture. Twenty-four hours later, 10 plasma clots thus labeled were pooled and washed twice with phosphate-buffered saline. Three milligrams o...

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Section: Methodsmentioning

confidence: 95%

Proportion of fetal hemoglobin synthesis decreases during erythroid cell maturation.

Chui¹,

Wong²,

Enkin³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

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“…14,15 Over the past decade, several lines of evidence have indicated that erythropoietin and EPOR exhibit a widespread distribution among a variety of organs in addition to kidney. [15][16][17][18] A large body of additional studies has shown that erythropoietin protects cardiac function by increasing blood flow and preventing apoptosis in ischemia models.…”

Section: Discussionmentioning

confidence: 99%

“…14,15 Erythropoietin and its receptor, erythropoietin receptor (EPOR), are expressed in a variety of tissues, including the vascular system. 16 -18 Beside its role in erythropoiesis, increasing evidence suggests that erythropoietin exerts several extrahematopoietic protective effects for cardiovascular diseases.…”

Section: Clinical Perspective On P 1837mentioning

confidence: 99%

Erythropoietin Suppresses the Formation of Macrophage Foam Cells

Ching

et al. 2010

Circulation

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Background-In addition to the hematopoietic effect of erythropoietin, increasing evidence suggests that erythropoietin also exerts protective effects for cardiovascular diseases. However, the role of erythropoietin and its underlying mechanism in macrophage foam cell formation are poorly understood. Methods and Results-Compared with wild-type specimens, erythropoietin was increased in atherosclerotic aortas of apolipoprotein E-deficient (apoE Ϫ/Ϫ ) mice, mainly in the macrophage foam cells of the lesions. Erythropoietin levels in culture medium and macrophages were significantly elevated in response to oxidized low-density lipoprotein in a dose-dependent manner. Furthermore, erythropoietin markedly attenuated lipid accumulation in oxidized low-density lipoprotein-treated macrophages, a result that was due to an increase in cholesterol efflux. Erythropoietin treatment significantly increased ATP-binding cassette transporters (ABC) A1 and ABCG1 mRNA and protein levels without affecting protein expression of scavenger receptors, including scavenger receptor-A, CD36, and scavenger receptor-BI. The upregulation of ABCA1 and ABCG1 by erythropoietin resulted from liver X receptor ␣ activation, which was confirmed by its prevention on expression of ABCA1 and ABCG1 after pharmacological or small interfering RNA inhibition of liver X receptor ␣. Moreover, the erythropoietin-mediated attenuation on lipid accumulation was abolished by such inhibition. Finally, reduced lipid accumulation and marked increase in ABCA1 and ABCG1 were demonstrated in erythropoietin-overexpressed macrophages. Conclusion-Our data suggest that erythropoietin suppresses foam cell formation via the liver X receptor ␣-dependent upregulation of ABCA1 and ABCG1. (Circulation.

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“…21 It has been suggested that human erythroblasts undergo an additional mitosis. 22 To explore this issue, we cultured sorted pure erythroblasts at each of the 5 developmental stages and examined their ability to proliferate. The representative growth curves of these cells showed that while proerythroblasts continued to proliferate for 4 days and expanded approximately 18 times during this period (from 0.4 3 10 6 to 7.4 3 10 6 ), orthochromatic erythroblasts were not able to divide at all ( Figure 4C).…”

Section: Mitotic Capacity Of Erythroblast Populations At Distinct Devmentioning

confidence: 99%

Isolation and functional characterization of human erythroblasts at distinct stages: implications for understanding of normal and disordered erythropoiesis in vivo

Liu

Xue

et al. 2013

Blood

319

351

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Regulation of Erythropoiesis. Xx. Kinetics of Red Cell Production*

Cited by 89 publications

References 25 publications

Proportion of fetal hemoglobin synthesis decreases during erythroid cell maturation.

Proportion of fetal hemoglobin synthesis decreases during erythroid cell maturation.

Erythropoietin Suppresses the Formation of Macrophage Foam Cells

Isolation and functional characterization of human erythroblasts at distinct stages: implications for understanding of normal and disordered erythropoiesis in vivo

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