ArticleMolecular endocrinology (Baltimore, Md.)2010
Thyroid hormone antagonizes tumor necrosis factor-alpha signaling in pituitary cells through the induction of dual specificity phosphatase 1.
Article in Molecular endocrinology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Molecular Determinants of Thyroid Cancer Progression: Thyroid Hormone Signaling, the BRAF/MAPK Pathway, and Emerging miRNA Biomarkers.Biomedicines · 2026Review
- Thyroid Hormone Action by Genomic and Nongenomic Molecular Mechanisms.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Lack of canonical thyroid hormone receptor α signaling changes regulatory T cell phenotype in female mice.iScience · 2024Article
- Effects of Thyroid Hormones on Lipid Metabolism Pathologies in Non-Alcoholic Fatty Liver Disease.Biomedicines · 2022Review
- Thyroid hormones act as modulators of inflammation through their nuclear receptors.Frontiers in endocrinology · 2022Review
- Regulation of metabolic and transcriptional responses by the thyroid hormone in cellular models of murine macrophages.Frontiers in immunology · 2022Article
- Article
- Pyrimethamine Elicits Antitumor Effects on Prostate Cancer by Inhibiting the p38-NF-κB Pathway.Frontiers in pharmacology · 2020Article
- Thyroid Hormone Receptor β Inhibits Self-Renewal Capacity of Breast Cancer Stem Cells.Thyroid : official journal of the American Thyroid Association · 2020Article
- The ligand-bound thyroid hormone receptor in macrophages ameliorates kidney injury via inhibition of nuclear factor-κB activities.Scientific reports · 2017Article
- The Thyroid Hormone Receptors Inhibit Hepatic Interleukin-6 Signaling During Endotoxemia.Scientific reports · 2016Article
- Deciphering the regulatory logic of an ancient, ultraconserved nuclear receptor enhancer module.Molecular endocrinology (Baltimore, Md.) · 2015Article
- Dual specificity phosphatase 1 expression inversely correlates with NF-κB activity and expression in prostate cancer and promotes apoptosis through a p38 MAPK dependent mechanism.Molecular oncology · 2014Article
- Thyroid hormone signaling and adult neurogenesis in mammals.Frontiers in endocrinology · 2014Review
- Involvement of the cellular phosphatase DUSP1 in vaccinia virus infection.PLoS pathogens · 2013Article
- The thyroid hormone receptors as modulators of skin proliferation and inflammation.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pituitary function has been shown to be regulated by an increasing number of factors, including cytokines and hormones, such as TNFalpha and T(3). Both the proinflammatory cytokine TNFalpha and T(3) have been suggested to be involved in the maintenance of tissue homeostasis in the anterior pituitary gland. In this report we show that T(3) negatively interferes with MAPK p38 and nuclear factor-kappaB (NF-kappaB) activation by TNFalpha in GH4C1 cells. Our data demonstrate that MAPK p38 is specifically activated upon exposure to TNFalpha and that T(3) abolishes this activation in a time-dependent manner by a mechanism that involves the induction of the MAPK phosphatase, DUSP1. Our data show that the pool of up-regulated DUSP1 by T(3) is mainly localized to the cytosol, and that TNFalpha does not affect this localization. On the other hand, we show that T(3) impairs the activation of the NF-kappaB pathway induced by TNFalpha, producing a significant decrease in NF-kappaB-dependent transcription, phosphorylation of IkappaBalpha, translocation of p65/NF-kappaB to the nucleus, and p65/NF-kappaB transactivation potential. Interestingly, the overexpression of DUSP1 inhibits the NF-kappaB activation achieved by either TNFalpha or ectopic expression of the upstream inducer of MAPK p38. Conversely, DUSP1 depletion abrogates the inhibitory effect of T(3) on the induction of NF-kappaB-dependent transcription by TNFalpha. Overall, our results indicate that T(3) antagonizes TNFalpha signaling in rat pituitary tumor cells through the induction of DUSP1.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.