The DNA binding-independent function of the glucocorticoid receptor mediates repression of AP-1-dependent genes in skin
Open accessAbstract
The glucocorticoid receptor (GR) mediates the biological effects of glucocorticoids (GCs) through activation or repression of gene expression, either by DNA binding or via interaction with other transcription factors, such as AP-1. Work in tissue culture cells on the regulation of AP-1-dependent genes, such as collagenase (MMP-13) and stromelysin (MMP-3) has suggested that the antitumor and antiinflammatory activity of GCs is mediated, at least in part, by GR-mediated downmodulation of AP-1. Here, we have identified phorbol ester-induced expression of MMP-3 and MMP-13 in mouse skin as the first example of an in vivo system to measure negative interference between AP-1 and GR in the animal. Cell type-specific induction of these genes by tumor promoters is abolished by GCs. Importantly, this is also the case in GR(dim) mice expressing a DNA binding-defective mutant version of GR. In contrast, the newly identified target genes in skin, plasma glutathione peroxidase and HSP-27, were induced by GC in wild-type, but not in GR(dim) mice. Thus, these data suggest that the DNA binding-independent function of the GR is dispensable for repression of AP-1 activity in vivo and responsible for the antitumor promoting activity of GCs.
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Initial evidence suggested that classic transactivation by GRs was defective in GRdim mice and that this mechanism was required for the full range of GC immunosuppressive actions.
“Initial evidence suggested that classic transactivation by GRs was defective in these mice and that this mechanism was required for the full range of GC immunosuppressive actions (107, 108).”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [108]
In GRdim mice, NF-kappaB and AP-1 target genes can still be silenced by GCs.
“Contrastingly, other findings indicate that in GRdim mice NF-κB and AP-1 target genes can still be silenced by GCs (107, 108), that the GC-inducible gene MKP-1 is normally expressed in macrophages (82) and that irritant dermatitis can successfully be treated with GCs (22).”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [108]
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- Authors
- Tuckermann, J. P., Reichardt, H. M., Arribas, R., Richter, K. H., Schütz, G., & Angel, P.
- Affiliations
- German Cancer Research Center (DE)
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 1999-12-27
- Volume
- 147
- Issue
- 7
- Pages
- 1365-1370
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC2174255
- OpenAlex
- W2085944780
- Cited by
- 196
- References
- 34
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 6 · 2020: 7 · 2019: 3 · 2018: 3 · 2017: 3 · 2016: 1 · 2015: 7 · 2014: 7 · 2013: 10 · 2012: 12
- FWCI
- 6.54
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- glucocorticoid receptor, AP-1, transcriptional repression, matrix metalloproteinases, MMP-3, MMP-13, phorbol ester, tumor promotion, skin, glutathione peroxidase, HSP27, anti-inflammatory activity
- MeSH terms
- Animals, DNA-Binding Proteins, Enzyme Induction, Enzyme Repression, Female, Glutathione Peroxidase, Heat-Shock Proteins, Mice, Inbred C57BL, Neoplasm Proteins, Receptors, Glucocorticoid, Skin, Tetradecanoylphorbol Acetate, Collagenases, Mice, Knockout, Transcription Factor AP-1, Molecular Chaperones, Matrix Metalloproteinase 3, Matrix Metalloproteinases, Mice, Matrix Metalloproteinase 13
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