Cited by 102Hemoglobinopathies and Related DisordersHemoglobin structure and functionHematopoietic Stem Cell Transplantation

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Hydroxyurea increases fetal hemoglobin in cultured erythroid cells derived from normal individuals and patients with sickle cell anemia or beta-thalassemia

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Fibach, E, Burke, LP, Schechter, AN, Noguchi, CT, Rodgers, GP·1993·Blood

DOI 10.1182/blood.v81.6.1630.1630

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Abstract

Hydroxyurea (HU), an inhibitor of DNA synthesis, has been shown to increase fetal hemoglobin (HbF) levels in patients with sickle cell anemia and in some patients with beta-thalassemia. However, until now there have not been good in vitro model systems that simulate this effect for study of the molecular and cellular mechanism(s) involved in perturbing the normal ontogeny of the globin genes. We analyzed the cellular effects of HU using a two-phase liquid culture procedure (Fibach et al: Blood 73:100, 1989) in which human peripheral blood-derived progenitor cells undergo proliferation and differentiation. HU was found to have multiple effects on these cultured cells: (1) an increase in the proportion of HbF produced; (2) a decrease in cell number due to inhibition of cell proliferation; (3) an increase in hemoglobin content per cell (mean corpuscular hemoglobin [MCH]); and (4) an increase in cell size (mean corpuscular volume). The extent of these effects was related to the HU dose and time of addition. When added to cell cultures from normal individuals, 4 days following their exposure to erythropoietin (EPO), 100 mumol/L HU caused a 1.3- to 3.5-fold increase in the proportion of HbF, from 0.4% to 5.2% (mean 1.6) in untreated to 1.5% to 8.2% (mean 3.1) in HU-treated cultures and a 45% +/- 10% increase in MCH but only a 25% +/- 7% decrease in cell number on day 13. Cultures of cells derived from five patients with sickle cell anemia have shown a twofold to fivefold increase in the percentage of Hb F following addition of HU while four patients with beta-thalassemia showed a 1.3- to 6.2-fold increase. We believe that this primary cell culture procedure should prove useful in studying the cellular and molecular mechanisms of pharmacologic induction of HbF and might provide a valuable predictive assay system for evaluation of the response of individual patients with hemoglobinopathies to HU and similar agents.

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Authors: Fibach, E., Burke, L., Schechter, A., Noguchi, C., & Rodgers, G.
Affiliations: Hadassah Medical Center (IL)
Department of Hematology, Hadassah University Hospital, Jerusalem, Israel.
ORCID: Fibach, E
Venue: Blood
Publisher: American Society of Hematology
Published: 1993-03-15
Volume: 81
Issue: 6
Pages: 1630-1635
ISSN: 0006-4971 (ISSN-L)
1528-0020
DOI: 10.1182/blood.v81.6.1630.1630
OpenAlex: W324137543
Cited by: 102
References: 28
Citations by year: 2026: 1 · 2025: 1 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 3 · 2019: 3 · 2018: 2 · 2017: 2 · 2016: 3 · 2015: 1 · 2014: 2 · 2013: 5 · 2012: 1
FWCI: 3.10
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Blood (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Genetics (clinical) › Hemoglobinopathies and Related Disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Hemoglobin structure and function
Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
Keywords: hydroxyurea, fetal hemoglobin, sickle cell disease, beta-thalassemia, erythroid progenitor cells, erythropoiesis, globin gene regulation, erythropoietin, cell proliferation inhibition, hemoglobin levels, predictive assays, hemoglobinopathies
MeSH terms: Anemia, Sickle Cell, Cells, Cultured, Fetal Hemoglobin, Humans, Hydroxyurea, Erythroid Precursor Cells, beta-Thalassemia

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Hydroxyurea increases fetal hemoglobin in cultured erythroid cells derived from normal individuals and patients with sickle cell anemia or beta-thalassemia

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