Evidence map›Paper›PMID 25378524›Full record

ArticleGut2015

Epigenetic upregulation of metabotropic glutamate receptor 2 in the spinal cord attenuates oestrogen-induced visceral hypersensitivity.

Dong-Yuan Cao, Guang Bai, Yaping Ji, Richard J Traub

Abstract read
In one paragraph

Article in Gut, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Pathology of pain and its implications for therapeutic interventions.Signal transduction and targeted therapy · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. MeCP2 Epigenetic Silencing ofFrontiers in neuroscience · 2021
    Article
  20. Article
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

4 authors at 1 institution in 1 country.

Dong-Yuan CaoDepartment of Neural and Pain Sciences, University of Maryland School of Dentistry, UM Center to Advance Chronic Pain Research, Baltimore, Maryland, USA.
Guang BaiDepartment of Neural and Pain Sciences, University of Maryland School of Dentistry, UM Center to Advance Chronic Pain Research, Baltimore, Maryland, USA.
Yaping JiDepartment of Neural and Pain Sciences, University of Maryland School of Dentistry, UM Center to Advance Chronic Pain Research, Baltimore, Maryland, USA.
Richard J TraubDepartment of Neural and Pain Sciences, University of Maryland School of Dentistry, UM Center to Advance Chronic Pain Research, Baltimore, Maryland, USA.
University of Maryland, Baltimore · US

Funding

NEUROCHEMICAL MECHANISMS OF VISCERAL PAINR01NS037424 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI TRAUB, RICHARD J · 1999 to 2013
$3.5M
NINDS NIH HHS R01 NS037424NINDS NIH HHS R01 NS 37424
6 · The paper itself

Abstract

objectiveEpigenetic mechanisms are potential targets to relieve somatic pain. However, little is known whether epigenetic regulation interferes with visceral pain. Previous studies show that oestrogen facilitates visceral pain. This study aimed to determine whether histone hyperacetylation in the spinal cord could attenuate oestrogen-facilitated visceral pain.

designThe effect of the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) on the magnitude of the visceromotor response (VMR) to colorectal distention was examined in ovariectomised rats with/without oestrogen replacement. An additional interaction with the metabotropic glutamate receptor 2/3 (mGluR2/3) antagonist LY341495 was tested. The levels of acetylated histone and mGluR2 mRNA and protein were analysed. The binding of acetylated H3 and oestrogen receptor α (ERα) to the GRM2 promoter was measured by chromatin immunoprecipitation coupled with qPCR.

resultsIn ovariectomised rats, 17β-estradiol (E2), but not safflower oil, increased the magnitude of the VMR to colorectal distention. SAHA attenuated the E2-facilitated VMR, but had no effect in safflower oil-treated rats. Subsequent spinal administration of LY341495 reversed the antinociceptive effect of SAHA in E2 rats. In addition, SAHA increased mGluR2 mRNA and protein in the spinal dorsal horn following E2, but not vehicle, treatment. In contrast, neither E2 nor SAHA alone altered mGluR2 mRNA. SAHA increased binding of H3K9ac and ERα to the same regions of the GRM2 promoter in E2-SAHA-treated animals.

conclusionsHistone hyperacetylation in the spinal cord attenuates the pronociceptive effects of oestrogen on visceral sensitivity, suggesting that epigenetic regulation may be a potential approach to relieve visceral pain.

Indexed as

AcetylationAmino AcidsAnimalsDisease Models, AnimalEpigenesis, GeneticEstradiolEstrogensFemaleHistone Deacetylase InhibitorsHistonesHydroxamic AcidsNociceptionOvariectomyRatsRats, Sprague-DawleyReceptors, Metabotropic GlutamateAmino AcidsEstradiolEstrogensHistone Deacetylase InhibitorsHistonesHydroxamic AcidsLY 341495metabotropic glutamate receptor 2metabotropic glutamate receptor 3Receptors, Metabotropic GlutamateRNA, MessengerVorinostatXanthenesIRRITABLE BOWEL SYNDROMENEUROPHARMACOLOGYSEX STEROIDSVISCERAL HYPERSENSITIVITYVISCERAL NOCICEPTION

Identifiers

PMID25378524
PMCPMC4562903
OpenAlexW2160413040

What OpenQuestion holds

Textmetadata
LicenceTDM
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.