Cited by 233Cytokine Signaling Pathways and InteractionsBlood disorders and treatmentsHematopoietic Stem Cell Transplantation

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STAT3 controls myeloid progenitor growth during emergency granulopoiesis

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Zhang, Huiyuan, Nguyen-Jackson, Hoainam, Panopoulos, Athanasia D., Li, Haiyan S., Murray, Peter J., Watowich, Stephanie S.·2010·Blood

DOI 10.1182/blood-2009-12-259630PMC PMC2953883

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Abstract

Granulocyte colony-stimulating factor (G-CSF) mediates “emergency” granulopoiesis during infection, a process that is mimicked by clinical G-CSF use, yet we understand little about the intracellular signaling cascades that control demand-driven neutrophil production. Using a murine model with conditional deletion of signal transducer and activator of transcription 3 (STAT3) in bone marrow, we investigated the cellular and molecular mechanisms of STAT3 function in the emergency granulopoiesis response to G-CSF administration or infection with Listeria monocytogenes, a pathogen that is restrained by G-CSF signaling in vivo. Our results show that STAT3 deficiency renders hematopoietic progenitor cells and myeloid precursors refractory to the growth-promoting functions of G-CSF or L monocytogenes infection. STAT3 is necessary for accelerating granulocyte cell-cycle progression and maturation in response to G-CSF. STAT3 directly controls G-CSF–dependent expression of CCAAT-enhancer-binding protein β (C/EBPβ), a crucial factor in the emergency granulopoiesis response. Moreover, STAT3 and C/EBPβ coregulate c-Myc through interactions with the c-myc promoter that control the duration of C/EBPα occupancy during demand-driven granulopoiesis. These results place STAT3 as an essential mediator of emergency granulopoiesis by its regulation of transcription factors that direct G-CSF–responsive myeloid progenitor expansion.

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Self-citation

Authors: Zhang, H., Nguyen-Jackson, H., Panopoulos, A. D., Li, H. S., Murray, P. J., & Watowich, S. S.
Affiliations: The University of Texas MD Anderson Cancer Center (US)
St. Jude Children's Research Hospital (US)
ORCID: Zhang, Huiyuan
Panopoulos, Athanasia D.
Li, Haiyan S.
Murray, Peter J.
Watowich, Stephanie S.
Venue: Blood
Publisher: American Society of Hematology
Published: 2010-10-07
Volume: 116
Issue: 14
Pages: 2462-2471
ISSN: 0006-4971 (ISSN-L)
1528-0020
DOI: 10.1182/blood-2009-12-259630
PMC: PMC2953883
OpenAlex: W2041168245
Semantic Scholar: 911cf5f012ca2c41275c386f29013395eb9d6499
Cited by: 232
References: 50
Citations by year: 2026: 9 · 2025: 10 · 2024: 11 · 2023: 13 · 2022: 12 · 2021: 17 · 2020: 24 · 2019: 19 · 2018: 12 · 2017: 16 · 2016: 18 · 2015: 12 · 2014: 16 · 2013: 15 · 2012: 13
FWCI: 6.49
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Blood (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Cancer Institute (P30CA16672, T32CA009598, P30CA016672, T32 CA09598-16)
National Institute of Allergy and Infectious Diseases (R21AI073587, AI073587)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
Health Sciences › Medicine › Hematology › Blood disorders and treatments
Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
Keywords: STAT3, emergency granulopoiesis, granulocyte colony-stimulating factor, myeloid progenitor cells, neutrophil production, Listeria monocytogenes infection, C/EBPβ, c-Myc, C/EBPα, cell cycle progression, transcriptional regulation, bone marrow
MeSH terms: Animals, Cell Cycle, Gene Expression Regulation, Granulocytes, Hematopoietic Stem Cells, Listeria monocytogenes, Promoter Regions, Genetic, Signal Transduction, Granulocyte Colony-Stimulating Factor, Proto-Oncogene Proteins c-myc, Leukopoiesis, CCAAT-Enhancer-Binding Proteins, CCAAT-Enhancer-Binding Protein-beta, STAT3 Transcription Factor, Mice

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STAT3 controls myeloid progenitor growth during emergency granulopoiesis

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