Evidence map›Paper›PMID 32961913›Full record

ArticleAntioxidants (Basel, Switzerland)2020

The Transcriptomic Response of the Murine Thyroid Gland to Iodide Overload and the Role of the Nrf2 Antioxidant System.

Dionysios V Chartoumpekis, Panos G Ziros, Ilias Georgakopoulos-Soares, Adam A T Smith, Ana Claudia Marques, Mark Ibberson, Peter A Kopp, Ioannis Habeos, Ioannis P Trougakos, Nicholas K H Khoo and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Keap1/Nrf2 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2021
    Article
  7. Review
  8. The Keap1/Nrf2 Signaling Pathway in the Thyroid-2020 Update.Antioxidants (Basel, Switzerland) · 2020
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 6 institutions in 3 countries.

Dionysios V ChartoumpekisService of Endocrinology and Diabetology, Lausanne University Hospital, and Faculty of Biology and Medicine, University of Lausanne, 1011 Lausanne, Switzerland.ORCID 0000-0002-6139-6067
Panos G ZirosService of Endocrinology and Diabetology, Lausanne University Hospital, and Faculty of Biology and Medicine, University of Lausanne, 1011 Lausanne, Switzerland.
Ilias Georgakopoulos-SoaresDepartment of Bioengineering and Therapeutic Sciences, University of California, San Francisco, San Francisco, CA 94158, USA.ORCID 0000-0003-3641-1488
Adam A T SmithDepartment of Computational Biology, University of Lausanne, 1015 Lausanne, Switzerland.ORCID 0000-0003-4593-3042
Ana Claudia MarquesDepartment of Computational Biology, University of Lausanne, 1015 Lausanne, Switzerland.
Mark IbbersonVital-IT Group, Swiss Institute of Bioinformatics, 1015 Lausanne, Switzerland.
Peter A KoppService of Endocrinology and Diabetology, Lausanne University Hospital, and Faculty of Biology and Medicine, University of Lausanne, 1011 Lausanne, Switzerland.
Ioannis HabeosDivision of Endocrinology, Department of Internal Medicine, University of Patras, 26504 Patras, Greece.
Ioannis P TrougakosDepartment of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, 15784 Athens, Greece.ORCID 0000-0002-6179-2772
Nicholas K H KhooDepartment of Pharmacology & Chemical Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Gerasimos P SykiotisService of Endocrinology and Diabetology, Lausanne University Hospital, and Faculty of Biology and Medicine, University of Lausanne, 1011 Lausanne, Switzerland.ORCID 0000-0002-9565-4941
University of Lausanne · CHUniversity of Patras · GRNational and Kapodistrian University of Athens · GRSIB Swiss Institute of Bioinformatics · CHUniversity of California, San Francisco · USUniversity of Pittsburgh · US

Funding

European Cooperation in Science and Technology CA16112Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 31003A_153062, 31003A_182105, IZSEZ0_193623 and IZCOZ0_177070Section/Board of Endocrinology of the European Union of Medical Specialists (UEMS) Exchange in Endocrinology Expertise (3E) Fellowshipthe Leenaards Foundation 2016 Fellowship for Academic Promotion in Clinical Medicine
6 · The paper itself

Abstract

backgroundThyroid follicular cells have physiologically high levels of reactive oxygen species because oxidation of iodide is essential for the iodination of thyroglobulin (Tg) during thyroid hormone synthesis. Thyroid follicles (the functional units of the thyroid) also utilize incompletely understood autoregulatory mechanisms to defend against exposure to excess iodide. To date, no transcriptomic studies have investigated these phenomena in vivo. Nuclear erythroid factor 2 like 2 (Nrf2 or Nfe2l2) is a transcription factor that regulates the expression of numerous antioxidant and other cytoprotective genes. We showed previously that the Nrf2 pathway regulates the antioxidant defense of follicular cells, as well as

methodsC57BL6/J wild-type (WT) or Nrf2 knockout (KO) male mice were administered regular water or water supplemented with 0.05% sodium iodide for seven days. RNA from their thyroids was prepared for next-generation RNA sequencing (RNA-Seq). Gene expression changes were assessed and pathway analyses were performed on the sets of differentially expressed genes.

resultsAnalysis of differentially expressed messenger RNAs (mRNAs) indicated that iodide overload upregulates inflammatory-, immune-, fibrosis- and oxidative stress-related pathways, including the Nrf2 pathway. Nrf2 KO mice showed a more pronounced inflammatory-autoimmune transcriptional response to iodide than WT mice. Compared to previously published datasets, the response patterns observed in WT mice had strong similarities with the patterns typical of Graves' disease and papillary thyroid carcinoma (PTC). Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) also responded to iodide overload, with the latter targeting mRNAs that participate mainly in inflammation pathways.

conclusionsIodide overload induces the Nrf2 cytoprotective response and upregulates inflammatory, immune, and fibrosis pathways similar to autoimmune hyperthyroidism (Graves' disease) and PTC.

Indexed as

fibrosisimmune responseinflammationiodineKelch-like ECH-associated protein 1 (Keap1)Nfe2l2oxidative stressRNA-Seq

Identifiers

PMID32961913
PMCPMC7555824
OpenAlexW3087505909

What OpenQuestion holds

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Registered trials

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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.