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C/EBPβ is required for 'emergency' granulopoiesis
Abstract
During 'emergency' situations such as infections, host defense requires rapid mobilization of bone marrow granulocyte progenitors. 'Steady-state' granulopoiesis is absolutely dependent on the C/EBPalpha transcription factor, but the transcriptional mechanisms underlying emergency granulopoiesis remain unclear. Here we show that large numbers of granulocytes were generated from C/EBPalpha-deficient progenitors after cytokine stimulation in vivo. Cytokine treatment or fungal infection induced upregulation of C/EBPbeta but not C/EBPalpha or C/EBPepsilon transcripts in granulocyte progenitors, and C/EBPbeta-deficient progenitors showed decreased emergency-induced granulopoiesis in vitro and in vivo. C/EBPbeta inhibited proliferation less severely than did C/EBPalpha. These data suggest a critical function for C/EBPbeta in emergency granulopoiesis, which demands both differentiation and proliferation of granulocyte precursors.
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“granulocyte cell-stimulating factor–mediated activation of STAT3 induces granulocytic progenitor proliferation through transcriptional upregulation of CCAAT/enhancer-binding protein (C/EBP)β and c-Myc”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Hirai et al., 2006
In the citing paper
“The mechanisms regulating “emergency” myelopoiesis are likely multifactorial, and transcriptional regulators such as C/EBPβ have also been implicated as drivers of hematopoietic responses to injury and infection (Hirai et al., 2006; Hirai et al., 2015).”
From PU.1 is required to restrain myelopoiesis during chronic inflammatory stress (2023) · cites this paper as Hirai et al., 2006
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Metadata
- Authors
- Hirai, H., Zhang, P., Dayaram, T., Hetherington, C. J., Mizuno, S.-I., Imanishi, J., Akashi, K., & Tenen, D. G.
- Affiliations
- Harvard University (US)
- Kyushu University (JP)
- Corresponding author
- Tenen, Daniel G
- Venue
- Nature Immunology
- Published
- 2006-06-04
- Volume
- 7
- Issue
- 7
- Pages
- 732-739
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- OpenAlex
- W1986957385
- Cited by
- 425
- References
- 61
- Citations by year
- 2026: 23 · 2025: 22 · 2024: 29 · 2023: 24 · 2022: 15 · 2021: 22 · 2020: 32 · 2019: 19 · 2018: 21 · 2017: 21 · 2016: 24 · 2015: 25 · 2014: 22 · 2013: 23 · 2012: 20
- FWCI
- 7.73
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL056745, HL56745)
- Topics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Hematology › Blood disorders and treatments
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- C/EBPβ, emergency granulopoiesis, C/EBPα, granulocyte progenitors, transcription factors, cytokine induction, fungal infection, granulocytic differentiation, progenitor cell proliferation
- MeSH terms
- Animals, Candidiasis, Cell Cycle, Cell Differentiation, Cells, Cultured, Colony-Forming Units Assay, Estradiol, Granulocytes, Hematopoiesis, Hematopoietic Stem Cells, Humans, Infections, Interleukin-3, Mice, Inbred C57BL, Radiation Chimera, Receptors, Estrogen, Recombinant Fusion Proteins, Transduction, Genetic, Up-Regulation, Granulocyte-Macrophage Colony-Stimulating Factor, Granulocyte Colony-Stimulating Factor, K562 Cells, Animals, Congenic, CCAAT-Enhancer-Binding Proteins, CCAAT-Enhancer-Binding Protein-alpha, CCAAT-Enhancer-Binding Protein-beta, Mice
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