The Proinflammatory Cytokine, Interleukin-1α, Reduces Glucocorticoid Receptor Translocation and Function1
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IL-1-α treatment is associated with significant upregulation of GR protein that is primarily apparent in the cytosolic compartment.
“IL-1-α treatment was also associated with significant upregulation of GR protein that was primarily apparent in the cytosolic compartment.43”
From Cytokines and Glucocorticoid Receptor Signaling (2009) · cites this paper as [43]
In a mouse L929 fibroblast cell line, administration of IL-1-α induces a significant decrease in DEX-induced GR translocation from cytoplasm to nucleus that is associated with decreased GR-DNA binding and decreased DEX-induced activation of a reporter gene construct with multiple glucocorticoid response elements (GRE) upstream of its promoter region.
“Using a mouse L929 fibroblast cell line, administration of IL-1-α was found to induce a significant decrease in DEX-induced GR translocation from cytoplasm to nucleus that was associated with decreased GR-DNA binding and decreased DEX-induced activation of a reporter gene construct with multiple glucocorticoid response elements (GRE) upstream of its promoter region.43”
From Cytokines and Glucocorticoid Receptor Signaling (2009) · cites this paper as [43]
Effects of IL-1-α on GR function were reversed by co-administration of IL-1 receptor antagonist (IL-1ra).
“Effects were reversed by co-administration of IL-1 receptor antagonist (IL-1ra).”
From Cytokines and Glucocorticoid Receptor Signaling (2009) · cites this paper as [43]
IL-1 inhibits the translocation of the glucocorticoid receptor from the cytoplasm into the cell nucleus and GR-mediated gene transcription.
“In support of this, IL-1 inhibits the translocation of the GR from the cytoplasm into the cell nucleus and GR-mediated gene transcription[39].”
From Neuroinflammation and cytokine abnormality in major depression: cause or consequence in that illness? (2016) · cites this paper as [39]
Cytokines directly affect glucocorticoid receptor function and induce glucocorticoid resistance.
“These findings suggest that cytokines directly affect GR function and induce glucocorticoid resistance.”
From Neuroinflammation and cytokine abnormality in major depression: cause or consequence in that illness? (2016) · cites this paper as [39]
Inflammatory cytokines and signalling pathways including MAPK, NF-kappaB, STAT, and cyclooxygenase inhibit glucocorticoid receptor function by acting on receptor translocation or receptor-mediated gene transcription.
“Inflammatory cytokines and their signalling pathways including MAPK, NF-kappaB, signal transducers and activators of transcription and cyclooxygenase have been found to inhibit GR function by acting on GR translocation or on GR-mediated gene transcription”
From Glucocorticoids, cytokines and brain abnormalities in depression (2011) · cites this paper as Pariante et al., 1999
Incubating L929 mouse fibroblasts with the pro-inflammatory cytokine IL-1 leads to glucocorticoid resistance, i.e., impairment of GR activation and translocation from the cytoplasm to the nucleus, resulting in reduced expression of GR-stimulated genes.
“we found that incubating L929 mouse fibroblasts cells with the pro-inflammatory cytokine interleukin (IL)-1 leads to glucocorticoid resistance, i.e., to an impairment of GR activation and translocation from the cytoplasm to the nucleus, resulting in reduced expression of GR-stimulated genes (Pariante et al., 1999).”
From Why are depressed patients inflamed? A reflection on 20 years of research on depression, glucocorticoid resistance and inflammation (2017) · cites this paper as Pariante et al., 1999
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Horowitz, M. A., Zunszain, P. A., Anacker, C., Musaelyan, K., & Pariante, C. M. (2013) · Modern Trends in Psychiatry · doi:10.1159/000343980 · Cited by 57 · see citing works
Self-citationWang, X., Wu, H., Lakdawala, V. S., Hu, F., Hanson, N. D., & Miller, A. H. (2004) · Neuropsychopharmacology · doi:10.1038/sj.npp.1300606 · Cited by 57 · see citing works
Self-citationPariante, C. M., Pearce, B., Pisell, T. L., Su, C., & Miller, A. (2001) · Journal of Endocrinology · doi:10.1677/joe.0.1690309 · Cited by 57 · see citing works
Self-citationHasegawa, T., Noda, K., Kumamoto, S., Ando, Y., Yamada, A., & Yoshikai, Y. (2000) · International Journal of Immunopharmacology · doi:10.1016/s0192-0561(00)00049-7 · Cited by 55 · see citing works
- Authors
- Pariante, C. M., Pearce, B. D., Pisell, T. L., Sanchez, C. I., Po, C., Su, C., & Miller, A. H.
- Corresponding author
- Pariante, Carmine M.
- ORCID
- Pariante, Carmine M.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 1999-09
- Volume
- 140
- Issue
- 9
- Pages
- 4359-4366
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W4238812515
- Cited by
- 40
- References
- 0
- Citations by year
- 2024: 1 · 2016: 1 · 2014: 1 · 2013: 2 · 2012: 4
- FWCI
- 1.22
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- interleukin-1, inflammatory cytokines, glucocorticoid receptor, receptor translocation, glucocorticoid signaling, inflammation, glucocorticoid resistance
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