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Cited by 32NF-κB Signaling PathwaysNeuropeptides and Animal PhysiologyThyroid Disorders and Treatments

NFκB Signaling Is Essential for the Lipopolysaccharide-Induced Increase of Type 2 Deiodinase in Tanycytes

de Vries, E.M., Kwakkel, J., Eggels, L., Kalsbeek, A., Barrett, P., Fliers, E., Boelen, A.·2014·Endocrinology
DOI 10.1210/en.2013-2018
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Abstract

The enzyme type 2 deiodinase (D2) is a major determinant of T3 production in the central nervous system. It is highly expressed in tanycytes, a specialized cell type lining the wall of the third ventricle. During acute inflammation, the expression of D2 in tanycytes is up-regulated by a mechanism that is poorly understood at present, but we hypothesized that cJun N-terminal kinase 1 (JNK1) and v-rel avian reticuloendotheliosis viral oncogene homolog A (RelA) (the 65 kD subunit of NFκB) inflammatory signal transduction pathways are involved. In a mouse model for acute inflammation, we studied the effects of lipopolysaccharide (LPS) on mRNA expression of D2, JNK1, and RelA in the periventricular area (PE) and the arcuate nucleus-median eminence of the hypothalamus. We next investigated LPS-induced D2 expression in primary tanycyte cell cultures. In the PE, the expression of D2 was increased by LPS. In the arcuate nucleus, but not in the PE, we found increased RelA mRNA expression. Likewise, LPS increased D2 and RelA mRNA expression in primary tanycyte cell cultures, whereas JNK1 mRNA expression did not change. Phosphorylation of RelA and JNK1 was increased in tanycyte cell cultures 15–60 minutes after LPS stimulation, confirming activation of these pathways. Finally, inhibition of RelA with the chemical inhibitors sulfasalazine and 4-Methyl-N1-(3-phenylpropyl)benzene-1,2-diamine (JSH-23) in tanycyte cell cultures prevented the LPS-induced D2 increase. We conclude that NFκB signaling is essential for the up-regulation of D2 in tanycytes during inflammation.

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  • Inhibition of RelA prevents the LPS-induced DIO2 increase in a cell culture of primary tanycytes, while tanycyte-specific knock down of RelA in mice showed that NF-κB is essential for the LPS-induced hypothalamic DIO2 increase and TRH decrease in vivo.

    “Inhibition of RelA prevents the LPS-induced DIO2 increase in a cell culture of primary tanycytes [63], while tanycyte-specific knock down of RelA in mice showed that NF-κB is essential for the LPS-induced hypothalamic DIO2 increase and TRH decrease in vivo [64].”

    From An update on non-thyroidal illness syndrome (2021) · cites this paper as [63]

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Authors
de Vries, E. M., Kwakkel, J., Eggels, L., Kalsbeek, A., Barrett, P., Fliers, E., & Boelen, A.
Affiliations
  • Department of Endocrinology and Metabolism (E.M.V., J.K., L.E., A.K., E.F., A.B.), Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands;
  • Amsterdam UMC Location University of Amsterdam (NL)
  • Netherlands Institute for Neuroscience (NL)
  • University of Aberdeen (GB)
Corresponding author
Boelen, A.
ORCID
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2014-05-01
Volume
155
Issue
5
Pages
2000-2008
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
DOI
10.1210/en.2013-2018
OpenAlex
W2079359536
Cited by
32
References
37
Citations by year
2026: 1 · 2025: 3 · 2024: 1 · 2023: 1 · 2022: 4 · 2021: 1 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 5 · 2016: 4 · 2015: 6
FWCI
1.60
Type
journal article
Language
en
Open access
closed
Locations
  • Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
  • KNAW Research Portal (The Royal Netherlands Academy of Arts and Sciences) (publishedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
  • Pure Amsterdam UMC (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
Keywords
NF-κB signaling, type 2 deiodinase, tanycytes, lipopolysaccharide, RelA, JNK1, acute inflammation, hypothalamus, arcuate nucleus, median eminence, sulfasalazine, JSH-23, protein phosphorylation
MeSH terms
Iodothyronine Deiodinase Type II, Animals, Arcuate Nucleus of Hypothalamus, Cells, Cultured, Endotoxins, Enzyme Induction, Female, Iodide Peroxidase, Male, Median Eminence, Nerve Tissue Proteins, Signal Transduction, NF-kappa B, Rats, Wistar, Midline Thalamic Nuclei, Mitogen-Activated Protein Kinase 8, Mice, Rats, Transcription Factor RelA, Mice, 129 Strain, Ependymoglial Cells

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