Characterization of the Nuclear Factor-κB Responsiveness of the Human dio2 Gene
Abstract
Type 2 iodothyronine deiodinase (D2) activates T4 by deiodination to T3, a process being the source of most T3 present in the brain. In the mediobasal hypothalamus, expression of the dio2 gene is potently activated by administration of bacterial lipopolysaccharide (LPS), which in turn mediates the modifications in thyroid homeostasis typically observed in patients with nonthyroidal illness syndrome. Here we show that LPS-induced D2 expression is also observed in human MSTO-211H cells that endogenously express D2. Exposure to LPS rapidly doubled D2 activity by a mechanism that was partially blocked by the nuclear factor-κB (NF-κB) inhibitor sulfasalazine. Next, the human dio2 5′-flanking region promoter assay was used in HC11 cells and the p65/NF-κB responsiveness mapped to the 3′ approximately 600-bp region of hdio2 5′-flanking region, with an approximately 15-fold induction. Semiquantitative EMSA identified the strongest NF-κB binding sites at the positions −683 bp (called no. 2) and −198 bp (no. 5) 5′ to the transcriptional starting site. Despite the very similar NF-κB binding affinity of these two sites, site-directed mutagenesis and promoter assay indicated that only site no. 5 possessed transactivation potency in the presence of the p65 subunit of NF-κB. Other cytokine mediators such as signal transducer and activator of transcription-3 (STAT3) or signal transducer and activator of transcription-5 (STAT5) did not induce transcription of the dio2 gene. Our results indicate that inflammatory signals regulate D2 expression predominantly via the NF-κB pathway in a direct transcriptional manner and could contribute to the changes in thyroid economy observed in nonthyroidal illness syndrome during infection.
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The 65kD subunit of NF-κB (RelA) activates the Dio2 promoter.
“The NF-κB protein family consists of several subunits of which the 65kD subunit of NF-κB (RelA) activates the Dio2 promoter [16, 62].”
From An update on non-thyroidal illness syndrome (2021) · cites this paper as [62]
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- Authors
- Zeöld, A., Doleschall, M., Haffner, M. C., Capelo, L. P., Menyhért, J., Liposits, Z., da Silva, W. S., Bianco, A. C., Kacskovics, I., Fekete, C., & Gereben, B.
- Affiliations
- Laboratory of Endocrine Neurobiology (A.Z., J.M., Z.L., C.F., B.G.), Faculty of Information Technology, Péter Pázmány Catholic University, Budapest H-1083, Hungary
- Department of Physiology and Biochemistry (M.D., I.K.), Faculty of Veterinary Science, Szent István University, H-1400 Budapest, Hungary
- Innsbruck Medical University (AT)
- Brigham and Women's Hospital (US)
- Pázmány Péter Catholic University (HU)
- Thyroid Section (L.P.C., W.S.d.S., A.C.B.), Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts 02115
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2006-09-01
- Volume
- 147
- Issue
- 9
- Pages
- 4419-4429
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2166955253
- Cited by
- 72
- References
- 60
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 3 · 2018: 1 · 2017: 1 · 2016: 5 · 2015: 6 · 2014: 6 · 2013: 6 · 2012: 3
- FWCI
- 3.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Hungarian Scientific Research Fund (T046492)
- National Institutes of Health
- Medical Research Council
- Fogarty International Center (TW006467, R03TW006467)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 65055, R01DK065055)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- type 2 deiodinase, NF-κB, p65 subunit, lipopolysaccharide, low T3 syndrome, thyroid hormone metabolism, transcriptional regulation, NF-kappaB binding site, STAT3, STAT5, inflammation, hypothalamus, sulfasalazine
- MeSH terms
- Iodothyronine Deiodinase Type II, Animals, Binding Sites, DNA, Gene Expression Regulation, Humans, Iodide Peroxidase, Lipopolysaccharides, Luciferases, Mesothelioma, Promoter Regions, Genetic, Recombinant Fusion Proteins, Sulfasalazine, Transcription, Genetic, Signal Transduction, Transcriptional Activation, Mutagenesis, Site-Directed, Cell Line, Tumor, STAT3 Transcription Factor, STAT5 Transcription Factor, Rats, Transcription Factor RelA
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