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Antiinflammatory effects of dexamethasone are partly dependent on induction of dual specificity phosphatase 1
Open accessAbstract
Glucocorticoids (GCs), which are used in the treatment of immune-mediated inflammatory diseases, inhibit the expression of many inflammatory mediators. They can also induce the expression of dual specificity phosphatase 1 (DUSP1; otherwise known as mitogen-activated protein kinase [MAPK] phosphatase 1), which dephosphorylates and inactivates MAPKs. We investigated the role of DUSP1 in the antiinflammatory action of the GC dexamethasone (Dex). Dex-mediated inhibition of c-Jun N-terminal kinase and p38 MAPK was abrogated in DUSP1-/- mouse macrophages. Dex-mediated suppression of several proinflammatory genes (including tumor necrosis factor, cyclooxygenase 2, and interleukin 1alpha and 1beta) was impaired in DUSP1-/- mouse macrophages, whereas other proinflammatory genes were inhibited by Dex in a DUSP1-independent manner. In vivo antiinflammatory effects of Dex on zymosan-induced inflammation were impaired in DUSP1-/- mice. Therefore, the expression of DUSP1 is required for the inhibition of proinflammatory signaling pathways by Dex in mouse macrophages. Furthermore, DUSP1 contributes to the antiinflammatory effects of Dex in vitro and in vivo.
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“GR-mediated transactivation typically induces the expression of potent signaling inhibitors (e.g., IκBα, MPK-1, IL-10, Annexin A1, GILZ, and SOCS proteins), which strongly interfere with salient immune signaling pathways such as those triggered by the Toll-like receptors (TLR) (82–85).”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [82]
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Metadata
- Authors
- Abraham, S. M., Lawrence, T., Kleiman, A., Warden, P., Medghalchi, M., Tuckermann, J., Saklatvala, J., & Clark, A. R.
- Affiliations
- Imperial College London (GB)
- Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) (DE)
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2006-07-31
- Volume
- 203
- Issue
- 8
- Pages
- 1883-1889
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2118371
- OpenAlex
- W2159379486
- Cited by
- 430
- References
- 29
- Citations by year
- 2026: 9 · 2025: 16 · 2024: 12 · 2023: 22 · 2022: 12 · 2021: 19 · 2020: 12 · 2019: 17 · 2018: 13 · 2017: 21 · 2016: 23 · 2015: 24 · 2014: 33 · 2013: 27 · 2012: 28
- FWCI
- 11.27
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion, other-oa)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- dexamethasone, glucocorticoids, MKP-1, MAPK phosphatase, macrophages, c-Jun N-terminal kinase, p38 MAPK, pro-inflammatory gene expression, TNF-α, cyclooxygenase-2, interleukin-1, zymosan-induced inflammation, MAPK dephosphorylation
- MeSH terms
- Animals, Anti-Inflammatory Agents, Bone Marrow, Dexamethasone, Dose-Response Relationship, Drug, Enzyme Induction, Gene Expression Regulation, Glucocorticoids, Inflammation, Macrophages, Phosphoprotein Phosphatases, RNA, Messenger, Signal Transduction, Protein Tyrosine Phosphatases, Immediate-Early Proteins, Cell Cycle Proteins, JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases, Mice, Dual Specificity Phosphatase 1, Protein Phosphatase 1
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