ArticleBlood2020
Understanding heterogeneity of fetal hemoglobin induction through comparative analysis of F and A erythroblasts.
Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 39 citations in OpenAlex.
- Global genetic modifiers of fetal hemoglobin in sickle cell disease: Systematic review and meta-analysis.iScience · 2026Article
- Genetic Contribution to Asthma Informs Acute Chest Syndrome Pathophysiology and Risk Stratification.American journal of hematology · 2026Article
- Epo and hypoxia accelerate a pattern of gradual cell cycle shortening in BFU-e and CFU-e erythroid progenitors in vivo.Blood advances · 2026Article
- Roxadustat induced fetal hemoglobin in anemic CKD patients: a dual-center real-world observational cohort study.BMC nephrology · 2026Observational
- p27Kip1 regulates γ-globin production.Blood · 2026Article
- Article
- The induction effect of hydroxyurea and metformin on fetal globin in the K562 cell line.Molecular medicine (Cambridge, Mass.) · 2025Article
- Detection of CRISPR/Cas9-Mediated Fetal Hemoglobin Reactivation in Erythroblasts Derived from Cord Blood-Hematopoietic Stem Cells.Molecular biotechnology · 2025Article
- Efficient andMolecular therapy. Nucleic acids · 2024Article
- CYB5R3 T117S tempers fetal hemoglobin induction by hydroxyurea in patients with sickle cell disease.Blood advances · 2024Article
- Transcriptional regulators of fetal hemoglobin.Hematology, transfusion and cell therapy · 2024Review
- Deformability of Heterogeneous Red Blood Cells in Aging and Related Pathologies.Aging and disease · 2024Review
- Article
- Saracatinib prompts hemin-induced K562 erythroid differentiation but suppresses erythropoiesis of hematopoietic stem cells.Human cell · 2024Article
- Development of a new staining protocol for the Kleihauer-Betke test to facilitate the reading of difficult cases.BMC pregnancy and childbirth · 2024Article
- Functional analysis of three new alpha-thalassemia deletions involving MCS-R2 reveals the presence of an additional enhancer element in the 5' boundary region.PLoS genetics · 2023Article
- Forced enhancer-promoter rewiring to alter gene expression in animal models.Molecular therapy. Nucleic acids · 2023Article
- HIC2 controls developmental hemoglobin switching by repressing BCL11A transcription.Nature genetics · 2022Article
- Development of a double shmiR lentivirus effectively targeting both BCL11A and ZNF410 for enhanced induction of fetal hemoglobin to treat β-hemoglobinopathies.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Microfluidic methods to advance mechanistic understanding and translational research in sickle cell disease.Translational research : the journal of laboratory and clinical medicine · 2022Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Reversing the developmental switch from fetal hemoglobin (HbF, α2γ2) to adult hemoglobin (HbA, α2β2) is an important therapeutic approach in sickle cell disease (SCD) and β-thalassemia. In healthy individuals, SCD patients, and patients treated with pharmacologic HbF inducers, HbF is present only in a subset of red blood cells known as F cells. Despite more than 50 years of observations, the cause for this heterocellular HbF expression pattern, even among genetically identical cells, remains unknown. Adult F cells might represent a reversion of a given cell to a fetal-like epigenetic and transcriptional state. Alternatively, isolated transcriptional or posttranscriptional events at the γ-globin genes might underlie heterocellularity. Here, we set out to understand the heterogeneity of HbF activation by developing techniques to purify and profile differentiation stage-matched late erythroblast F cells and non-F cells (A cells) from the human HUDEP2 erythroid cell line and primary human erythroid cultures. Transcriptional and proteomic profiling of these cells demonstrated very few differences between F and A cells at the RNA level either under baseline conditions or after treatment with HbF inducers hydroxyurea or pomalidomide. Surprisingly, we did not find differences in expression of any known HbF regulators, including BCL11A or LRF, that would account for HbF activation. Our analysis shows that F erythroblasts are not significantly different from non-HbF-expressing cells and that the primary differences likely occur at the transcriptional level at the β-globin locus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.