Evidence map›Paper›PMID 22434086›Full record

ArticleEndocrinology2012

The ERβ ligand 5α-androstane, 3β,17β-diol (3β-diol) regulates hypothalamic oxytocin (Oxt) gene expression.

Dharmendra Sharma, Robert J Handa, Rosalie M Uht

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
6.1field-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

28 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Complementary Role of Oxytocin and Vasopressin in Cardiovascular Regulation.International journal of molecular sciences · 2021
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Direct Involvement of Androgen Receptor in Oxytocin Gene Expression: Possible Relevance for Mood Disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
    Article
  13. Article
  14. Review
  15. 17PeerJ · 2017
    Article
  16. Article
  17. Article
  18. 5α-Reduced neurosteroids sex-dependently reverse central prenatal programming of neuroendocrine stress responses in rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  19. Review
  20. Autism, oxytocin and interoception.Neuroscience and biobehavioral reviews · 2014
    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

3 authors at 2 institutions in 1 country.

Dharmendra SharmaDepartment of Pharmacology and Neuroscience and Institute for Aging and Alzheimer's Disease Research, University of North Texas Health Science Center, Fort Worth, Texas 76107, USA.
Robert J Handa
Rosalie M Uht
University of North Texas Health Science Center · USUniversity of Arizona · US

Funding

SEX DIFFERENCES IN HYPOTHALAMO-PITUITARY-ADRENAL AXISR01NS039951 · NINDS · UNIVERSITY OF ARIZONA · PI HANDA, ROBERT J · 2001 to 2013
$4.3M
GR-Mediated Epigenetic Regulation of the CRH GeneR01MH082900 · NIMH · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI UHT, ROSALIE MARIE · 2009 to 2013
$1.8M
NIMH NIH HHS R01 MH082900NIMH NIH HHS R01-MH082900NINDS NIH HHS R01 NS039951NINDS NIH HHS R01-NS039951
6 · The paper itself

Abstract

The endocrine component of the stress response is regulated by glucocorticoids and sex steroids. Testosterone down-regulates hypothalamic-pituitary-adrenal (HPA) axis activity; however, the mechanisms by which it does so are poorly understood. A candidate testosterone target is the oxytocin gene (Oxt), given that it too inhibits HPA activity. Within the paraventricular nucleus of the hypothalamus, oxytocinergic neurons involved in regulating the stress response do not express androgen receptors but do express estrogen receptor-β (ERβ), which binds the dihydrotestosterone metabolite 3β,17β-diol (3β-diol). Testosterone regulation of the HPA axis thus appears to involve the conversion to the ERβ-selective ligand 5α-androstane, 3β-diol. To study mechanisms by which 3β-diol could regulate Oxt expression, we used a hypothalamic neuronal cell line derived from embryonic mice that expresses Oxt constitutively and compared 3β-diol with estradiol (E2) effects. E2 and 3β-diol elicited a phasic response in Oxt mRNA levels. In the presence of either ligand, Oxt mRNA levels were increased for at least 60 min and returned to baseline by 2 h. ERβ occupancy preceded an increase in Oxt mRNA levels in the presence of 3β-diol but not E2. In tandem with ERβ occupancy, 3β-diol increased occupancy of the Oxt promoter by cAMP response element-binding protein and steroid receptor coactivator-1 at 30 min. At the same time, 3β-diol led to the increased acetylation of histone H4 but not H3. Taken together, the data suggest that in the presence of 3β-diol, ERβ associates with cAMP response element-binding protein and steroid receptor coactivator-1 to form a functional complex that drives Oxt gene expression.

Indexed as

Androstane-3,17-diolAnimalsCell LineCells, CulturedEstradiolGene ExpressionHypothalamusMiceNeuronsOxytocinPromoter Regions, GeneticAndrostane-3,17-diolEstradiolOxytocin

Identifiers

PMID22434086
PMCPMC3339641
OpenAlexW2023010955

What OpenQuestion holds

Textmetadata
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.