Effects of testosterone and erythropoietin on erythroid colony formation in human bone marrow cultures
Abstract
The effects of testosterone and erythropoietin (ESF) on erythroid colony formation in normal human bone marrow cultures were studied in vitro using a methyl cellulose gel system. Testosterone was found to produce a significant increase in erythroid colony formation at concentrations of 10–4–10-4M in vitro. In this system, the numbers of erythroid colonies formed per plate increased in direct proportion to the increase in the number of erythroid precursors inoculated as well as to the increase in the dose of ESF in vitro. In addition, a synergistic effect of a combination of testosterone and ESF on erythroid colony formation was seen when ESF was present at high concentrations. These data suggest that a greater number of erythropoietin-responsive cells are available for ESF to differentiate into the nucleated erythroid cell line in the presence of testosterone, indicating that the effect of a combination of testosterone and ESF is greater in enhancing erythropoiesis than the additive effects of either agent alone.
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Genetic alterations in iron regulatory genes in mice (hamp knockout, ferroportin deletion mutant pcm mice) alone are sufficient to cause transient polycythemia.
“Nonetheless, genetic alterations in iron regulatory genes in mice (hamp knockout, ferroportin deletion mutant pcm mice) alone are sufficient to cause transient polycythemia, thus supporting the hypothesis that suppression of hepcidin by itself may play a contributory role in testosterone-induced erythrocytosis (28,29).”
From Testosterone induces erythrocytosis via increased erythropoietin and suppressed hepcidin: evidence for a new erythropoietin/hemoglobin set point (2014) · cites this paper as [29]
Suppression of hepcidin by itself may play a contributory role in testosterone-induced erythrocytosis.
“Nonetheless, genetic alterations in iron regulatory genes in mice (hamp knockout, ferroportin deletion mutant pcm mice) alone are sufficient to cause transient polycythemia, thus supporting the hypothesis that suppression of hepcidin by itself may play a contributory role in testosterone-induced erythrocytosis (28,29).”
From Testosterone induces erythrocytosis via increased erythropoietin and suppressed hepcidin: evidence for a new erythropoietin/hemoglobin set point (2014) · cites this paper as [29]
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Testosterone-Secreting Ovarian Tumor: A Rare Cause of Erythrocytosis and Pulmonary Embolus
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- Authors
- Moriyama, Y., & Fisher, J.
- Affiliations
- Tulane University (US)
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 1975-05-01
- Volume
- 45
- Issue
- 5
- Pages
- 665-670
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W156816576
- Cited by
- 100
- References
- 17
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 5 · 2022: 3 · 2021: 3 · 2020: 6 · 2019: 6 · 2018: 3 · 2017: 7 · 2016: 1 · 2015: 3 · 2014: 2 · 2013: 2 · 2012: 5
- FWCI
- 6.39
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal and reproductive studies
- Keywords
- testosterone, erythropoietin, erythroid colony formation, erythropoiesis, human bone marrow, synergistic effect, erythroid precursors
- MeSH terms
- Benzidines, Bone Marrow Cells, Cell Count, Cell Division, Cell Separation, Cells, Cultured, Culture Media, Erythrocytes, Erythropoiesis, Erythropoietin, Humans, Staining and Labeling, Testosterone
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