Inhibition of Erythropoiesis by Estrogens

Dukes, Peter P.; Goldwasser, Eugene

doi:10.1210/endo-69-1-21

Cited by 104 publications

(44 citation statements)

References 10 publications

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“…Especially, 17␤-estradiol (E 2 ), the plasma level of which gradually increases along with the progress of pregnancy and reaches as much as 30 ng/mL at term, around 100 times that of nonpregnant women, 14 has been well studied, with an inhibitory effect on Epo production reported in animal experiments. [15][16][17][18] However, the anemia observed in pregnancy is not derived from E 2 -induced insufficient Epo production, since actual RBC generation increases; the increase in plasma volume surpasses that in RBC mass (about 150% and 120% of those in a nonpregnant woman, respectively), resulting in "dilutional" or "physiologic" anemia. 19 The expansion of RBC volume is obviously derived from increased Epo production, even though it is somewhat suppressed by the large amount of endogenously secreted E 2 or diluted by the increase of plasma volume.…”

Section: Introductionmentioning

confidence: 99%

The effects of iron deficiency on estradiol-induced suppression of erythropoietin induction in rats: implications of pregnancy-related anemia

Horiguchi

Oguma

Kayama

2005

Blood

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Pregnant women often develop anemia concomitant with the increase in serum erythropoietin levels, which are actually lower than those of nonpregnant anemic women due to the possible suppressive effect of endogenous estradiol on erythropoietin induction. The anemia, derived from hemodilution, does not act as a drive for erythropoietin induction, but iron deficiency, often observed during pregnancy, might. In order to demonstrate this, we investigated the effects of iron deficiency on estradiol-induced suppression of erythropoietin induction in rats. Single doses of estradiol suppressed hypoxia-, cobalt-, and bleeding-stimulated elevation of plasma erythropoietin levels and renal erythropoietin mRNA expression. Repeated administration of estradiol at 0.1 and 1 mg/kg for 2 months induced a slight anemic trend without elevation of plasma erythropoietin. Feeding an iron-deficient diet for 2 months induced plasma erythropoietin elevation without obvious anemia, but the simultaneous repeated administration of estradiol suppressed it and reversed the iron deficiency. Plasma erythropoietin levels had distinct negative correlations with plasma iron, plasma ferritin, and iron concentrations in the organs, but not with plasma hemoglobin level. These results suggest that iron deficiency would significantly stimulate erythropoietin induction during pregnancy, although estradiol might suppress it through iron restoration. (Blood. 2005;106:67-74)

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Section: Introductionmentioning

confidence: 99%

The effects of iron deficiency on estradiol-induced suppression of erythropoietin induction in rats: implications of pregnancy-related anemia

Horiguchi

Oguma

Kayama

2005

Blood

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“…If operative in erythroid cells, this mechanism might account for some of the biological effects of estrogens on erythropoiesis. These include induction of anemia in mammals treated with high doses of estrogens (13,15,34,53), reduction of the number of human bone marrowderived erythroid progenitor cells grown in the presence of estrogens (3), and delay of maturation of chicken bone marrow-derived erythroid progenitor cells (45). In the latter case, the block in differentiation is associated with reduced expression of many erythroid-cell-expressed genes (45).…”

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confidence: 99%

Estrogen-Induced Apoptosis by Inhibition of the Erythroid Transcription Factor GATA-1

Blobel

Orkin

1996

Molecular and Cellular Biology

108

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Steroid hormones regulate diverse biological functions, including programmed cell death (apoptosis).Although steroid receptors have been studied extensively, relatively little is known regarding the cellular targets through which apoptosis is triggered. We show here that the ligand-activated estrogen receptor (ER) induces apoptosis in an erythroid cell line by binding to, and consequently inhibiting the activity of, GATA-1, an erythroid transcription factor essential for the survival and maturation of erythroid precursor cells. GATA-1 inhibition is reflected in the downregulation of presumptive GATA-1 target genes. Constitutive overexpression of a GATA-binding protein resistant to the effects of the ER partially rescues ER-induced apoptosis. Induction of apoptosis by a mutant ER defective in binding to the estrogen response element but active in GATA-1 inhibition suggests that ER-mediated inhibition of GATA-1 is direct and does not require estrogen response element-dependent transcriptional activation. Thus, a lineage-restricted transcription factor, such as GATA-1, constitutes one cellular target through which steroid hormones may control apoptosis. As GATA-binding proteins are evolutionarily conserved, we speculate that members of the steroid receptor family may exert some of their diverse biological functions in different cellular contexts through interference with the function of GATA-binding proteins.

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“…It is the fact that direct stimulatory effect of androgen in men in the bone marrow in association with erythropoietin, and an inhibitory effect of estrogen on the bone marrow in women [13,14]. The fact has been approved in vitro and understood that there was a direct link in vivo that androgens raised the hemoglobin levels in males and females [15][16][17]. It is another fact that the person`s hormones change with aging.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the Hemoglobin Amount between Old and Young Persons in Bosnia and Herzegovina

Dogan¹,

Mermer²

2017

J Biom Biostat

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Hemoglobin is a unique protein, which is responsible for oxygen and carbon dioxide transportation all the body. The protein location is inside the erythrocytes and the special oval shape makes it easily pass through blood walls to supply oxygen to the tissues and organs. It is supposed that the hemoglobin amount could change depending on the person`s age, gender or nationality. We designed a research to see the molecular differences among Bosnian and Turkish young person`s whose age interval is 18-23 and old person`s age interval is 43-65. Totally 300 person`s, 50 from each Bosnian/ Turkish Female/Male and 50 old male and 50 old female were selected for the research. The students` the hemoglobin amount has been recorded individually and presented in a table. As a result of the measurement, The Turkish females average has the lowest hemoglobin Turkish males average shows the maximum amount of hemoglobin, 12.01 g/dl and 14.65 g/dl respectively. When the female gets older their the hemoglobin amount increase in their blood, 7.3% in Bosnian and 12.2% in Turkish. On the other side, the male blood the hemoglobin amount is almost similar by aging, Bosnian male hemoglobin just increase 0.74%, but in Turkish male 1.3% decrease. The result shows that female the hemoglobin amount is affected by age more than male.

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Inhibition of Erythropoiesis by Estrogens

Cited by 104 publications

References 10 publications

The effects of iron deficiency on estradiol-induced suppression of erythropoietin induction in rats: implications of pregnancy-related anemia

The effects of iron deficiency on estradiol-induced suppression of erythropoietin induction in rats: implications of pregnancy-related anemia

Estrogen-Induced Apoptosis by Inhibition of the Erythroid Transcription Factor GATA-1

Comparison of the Hemoglobin Amount between Old and Young Persons in Bosnia and Herzegovina

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