C/EBPα determines hematopoietic cell fate in multipotential progenitor cells by inhibiting erythroid differentiation and inducing myeloid differentiation
Open accessAbstract
C/EBPα is an essential transcription factor required for myeloid differentiation. While C/EBPα can act as a cell fate switch to promote granulocyte differentiation in bipotential granulocyte-macrophage progenitors (GMPs), its role in regulating cell fate decisions in more primitive progenitors is not known. We found increased numbers of erythroid progenitors and erythroid cells in C/EBPα–/– fetal liver (FL). Also, enforced expression of C/EBPα in hematopoietic stem cells resulted in a loss of erythroid progenitors and an increase in myeloid cells by inhibition of erythroid development and inducing myeloid differentiation. Conditional expression of C/EBPα in murine erythroleukemia (MEL) cells induced myeloid-specific genes, while inhibiting erythroid-specific gene expression including erythropoietin receptor (EpoR), which suggests a novel mechanism to determine hematopoietic cell fate. Thus, C/EBPα functions in hematopoietic cell fate decisions by the dual actions of inhibiting erythroid and inducing myeloid gene expression in multipotential progenitors.
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Cebpa inhibits ME lineage differentiation.
“Cebpa promotes GM lineage differentiation while inhibiting ME lineage differentiation16,72, and promoting granulocyte differentiation in particular15.”
From Dissecting cell identity via network inference and in silico gene perturbation (2023) · cites this paper as [72]
Cebpa promotes granulocyte differentiation.
“Cebpa promotes GM lineage differentiation while inhibiting ME lineage differentiation16,72, and promoting granulocyte differentiation in particular15.”
From Dissecting cell identity via network inference and in silico gene perturbation (2023) · cites this paper as [72]
Cebpa promotes GM lineage differentiation.
“Cebpa promotes GM lineage differentiation while inhibiting ME lineage differentiation16,72, and promoting granulocyte differentiation in particular15.”
From Dissecting cell identity via network inference and in silico gene perturbation (2023) · cites this paper as [72]
Gfi1 promotes granulocyte lineage differentiation.
“Gfi1 promotes granulocyte lineage differentiation15,72–74.”
From Dissecting cell identity via network inference and in silico gene perturbation (2023) · cites this paper as [72]
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- Authors
- Suh, H. C., Gooya, J., Renn, K., Friedman, A. D., Johnson, P. F., & Keller, J. R.
- Affiliations
- Johns Hopkins University (US)
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2006-06-01
- Volume
- 107
- Issue
- 11
- Pages
- 4308-4316
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC1895788
- OpenAlex
- W2048645509
- Cited by
- 95
- References
- 54
- Citations by year
- 2026: 7 · 2025: 6 · 2024: 6 · 2023: 4 · 2022: 3 · 2021: 6 · 2020: 4 · 2019: 2 · 2018: 3 · 2017: 5 · 2016: 3 · 2015: 7 · 2014: 4 · 2013: 4 · 2012: 3
- FWCI
- 3.85
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Health and Human Services
- National Institutes of Health (n01co12400-79-0-22, NO1-CO12400)
- National Cancer Institute (N01CO12400, NO1‐CO‐12400)
- Topics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Keywords
- C/EBPα, erythroid differentiation, myeloid differentiation, hematopoietic stem cells, erythropoietin receptor, erythroid progenitor cells, CFU-GM, transcription factors, murine erythroleukemia cells, fetal liver
- MeSH terms
- Animals, Cell Count, Cell Differentiation, Cells, Cultured, Gene Expression Regulation, Hematopoiesis, Liver, Transfection, Receptors, Erythropoietin, Mice, Knockout, Myeloid Cells, CCAAT-Enhancer-Binding Protein-alpha, Multipotent Stem Cells, Erythroid Cells, Mice
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