Evidence map›Paper›PMID 24618783›Full record

ArticlePloS one2014

Thyroid hormone regulation of gene expression in primary cerebrocortical cells: role of thyroid hormone receptor subtypes and interactions with retinoic acid and glucocorticoids.

Pilar Gil-Ibáñez, Juan Bernal, Beatriz Morte

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 80 citations in OpenAlex.

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  9. Cardamom (International journal of molecular sciences · 2023
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  11. Review
  12. Article
  13. Review
  14. An Atlas of Thyroid Hormone Receptors' Target Genes in Mouse Tissues.International journal of molecular sciences · 2022
    Article
  15. Epigenetics of pregnancy: looking beyond the DNA code.Journal of assisted reproduction and genetics · 2022
    Review
  16. Review
  17. Article
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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

3 authors at 2 institutions in 1 country.

Pilar Gil-IbáñezInstituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas (CSIC), Madrid, Spain; Universidad Autónoma de Madrid (UAM), Madrid, Spain; Center for Biomedical Research On Rare Diseases (Ciberer), Instituto de Salud Carlos III, Madrid, Spain.
Juan BernalInstituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas (CSIC), Madrid, Spain; Universidad Autónoma de Madrid (UAM), Madrid, Spain; Center for Biomedical Research On Rare Diseases (Ciberer), Instituto de Salud Carlos III, Madrid, Spain.
Beatriz MorteInstituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas (CSIC), Madrid, Spain; Universidad Autónoma de Madrid (UAM), Madrid, Spain; Center for Biomedical Research On Rare Diseases (Ciberer), Instituto de Salud Carlos III, Madrid, Spain.
Instituto de Salud Carlos III · ESConsejo Superior de Investigaciones Científicas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The effects of thyroid hormone on brain development and function are largely mediated by the binding of 3,5,3'-triiodo-L-thyronine (T3) to its nuclear receptors (TR) to regulate positively or negatively gene expression. We have analyzed by quantitative polymerase chain reaction the effect of T3 on primary cultured cells from the embryonic mouse cerebral cortex, on the expression of Hr, Klf9, Shh, Dio3, Aldh1a1, and Aldh1a3. In particular we focused on T3 receptor specificity, and on the crosstalk between T3, retinoic acid and dexamethasone. To check for receptor subtype specificity we used cerebrocortical cells derived from wild type mice and from mice deficient in thyroid hormone receptor subtypes. Receptor subtype specificity was found for Dio3 and Aldh1a1, which were induced by T3 only in cells expressing the T3 receptor alpha 1 subtype. Interactions of T3 with retinoic acid signaling through the control of retinoic acid metabolism are likely to be important during development. T3 had opposing influences on retinoic acid synthesizing enzymes, increasing the expression of Aldh1a1, and decreasing Aldh1a3, while increasing the retinoic acid degrading enzyme Cyp26b1. Dexamethasone increased Klf9 and Aldh1a1 expression. The effects of T3 and dexamethasone on Aldh1a1 were highly synergistic, with mRNA increments of up to 20 fold. The results provide new data on thyroid hormone regulation of gene expression and underscore the importance of thyroid hormone interactions with retinoic acid and glucocorticoids during neural development.

Indexed as

Gene Expression RegulationAnimalsCells, CulturedCerebral CortexGlucocorticoidsMiceMice, KnockoutModels, BiologicalReceptors, Thyroid HormoneThyroid Hormone Receptors alphaThyroid Hormone Receptors betaThyroid HormonesTretinoinGlucocorticoidsReceptors, Thyroid HormoneThyroid Hormone Receptors alphaThyroid Hormone Receptors betaThyroid HormonesTretinoin

Identifiers

PMID24618783
PMCPMC3950245
OpenAlexW2042924921

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.