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Cited by 117Cytokine Signaling Pathways and InteractionsImmune cells in cancerNF-κB Signaling Pathways

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The JNK Are Important for Development and Survival of Macrophages

Himes, S Roy, Sester, David P, Ravasi, Timothy, Cronau, Stephen L, Sasmono, Tedjo, Hume, David A·2006·The Journal of Immunology
DOI 10.4049/jimmunol.176.4.2219
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Abstract

We report in this study that activation of the JNK by the growth factor, CSF-1 is critical for macrophage development, proliferation, and survival. Inhibition of JNK with two distinct classes of inhibitors, the pharmacological agent SP600125, or the peptide D-JNKI1 resulted in cell cycle inhibition with an arrest at the G2/M transition and subsequent apoptosis. JNK inhibition resulted in decreased expression of CSF-1R (c-fms) and Bcl-xL mRNA in mature macrophages and repressed CSF-1-dependent differentiation of bone marrow cells to macrophages. Macrophage sensitivity to JNK inhibitors may be linked to phosphorylation of the PU.1 transcription factor. Inhibition of JNK disrupted PU.1 binding to an element in the c-fms gene promoter and decreased promoter activity. Promoter activity could be restored by overexpression of PU.1. A comparison of expression profiles of macrophages with 22 other tissue types showed that genes that signal JNK activation downstream of tyrosine kinase receptors, such as focal adhesion kinase, Nck-interacting kinase, and Rac1 and scaffold proteins are highly expressed in macrophages relative to other tissues. This pattern of expression may underlie the novel role of JNK in macrophages.

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Metadata

Authors
Himes, S. R., Sester, D. P., Ravasi, T., Cronau, S. L., Sasmono, T., & Hume, D. A.
Affiliations
  • The University of Queensland (AU)
  • Cooperative Research Centre for Chronic Inflammatory Disease, Institute for Molecular Biosciences, University of Queensland , Brisbane ,
ORCID
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2006-02
Volume
176
Issue
4
Pages
2219-2228
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.176.4.2219
OpenAlex
W1582648966
Cited by
117
References
69
Citations by year
2026: 1 · 2025: 3 · 2024: 4 · 2023: 3 · 2022: 5 · 2021: 4 · 2020: 7 · 2019: 10 · 2018: 1 · 2017: 5 · 2016: 6 · 2015: 6 · 2014: 11 · 2013: 9 · 2012: 5
FWCI
3.24
Type
journal article
Language
en
Open access
closed
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
  • Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
JNK, macrophage development, macrophage survival, CSF-1, CSF-1 receptor, c-fms, Bcl-xL, apoptosis, cell cycle arrest, G2/M cell cycle arrest, PU.1, transcriptional regulation, macrophage differentiation, bone marrow, JNK inhibitor, SP600125, tyrosine kinase signaling, focal adhesion kinase, Rac1, scaffold proteins
MeSH terms
Proto-Oncogene Protein Spi-1, Animals, Bone Marrow Cells, Cell Differentiation, Cell Survival, Cells, Cultured, DNA, Gene Expression Regulation, Macrophages, Phosphorylation, Promoter Regions, Genetic, Protein Binding, Proto-Oncogene Proteins, RNA, Messenger, Signal Transduction, Trans-Activators, Macrophage Colony-Stimulating Factor, Receptor, Macrophage Colony-Stimulating Factor, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, JNK Mitogen-Activated Protein Kinases, Mice

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