Evidence map›Paper›PMID 27385724›Full record

ArticleMolecular pain2016

EXPRESS: Histone hyperacetylation modulates spinal type II metabotropic glutamate receptor alleviating stress-induced visceral hypersensitivity in female rats.

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

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. FOXD3-mediated transactivation of ALKBH5 promotes neuropathic pain via mProceedings of the National Academy of Sciences of the United States of America · 2024
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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

5 authors at 1 institution in 2 countries.

Dong-Yuan CaoUniversity of Maryland School of Dentistry.
Guang BaiUniversity of Maryland School of Dentistry.
Yaping JiUniversity of Maryland School of Dentistry.
Jane M KarpowiczUniversity of Maryland School of DentistryUniversity of Maryland School of DentistryUniversity of Maryland School of Dentistry.
Richard J TraubUniversity of Maryland School of DentistryUniversity of Maryland School of DentistryUniversity of Maryland School of Dentistry rtraub@umaryland.edu.
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 NS 37424
6 · The paper itself

Abstract

Stress is often a trigger to exacerbate chronic pain including visceral hypersensitivity associated with irritable bowel syndrome, a female predominant functional bowel disorder. Epigenetic mechanisms that mediate stress responses are a potential target to interfere with visceral pain. The purpose of this study was to examine the effect of a histone deacetylase inhibitor, suberoylanilide hydroxamic acid, on visceral hypersensitivity induced by a subchronic stressor in female rats and to investigate the involvement of spinal glutamate receptors. Three daily sessions of forced swim induced visceral hypersensitivity. Intrathecal suberoylanilide hydroxamic acid prevented or reversed the stress-induced visceral hypersensitivity, increased spinal histone 3 acetylation and increased mGluR2 and mGluR3 expression. Chromatin immunoprecipitation (ChIP) analysis revealed enrichment of H3K9Ac and H3K18Ac at several promoter Grm2 and Grm3 regions. The mGluR2/3 antagonist LY341495 reversed the inhibitory effect of suberoylanilide hydroxamic acid on the stress-induced visceral hypersensitivity. In surprising contrast, stress and/or suberoylanilide hydroxamic acid had no effect on spinal NMDA receptor expression or function. These data reveal histone modification modulates mGluR2/3 expression in the spinal cord to attenuate stressinduced visceral hypersensitivity. HDAC inhibitors may provide a potential approach to relieve visceral hypersensitivity associated with irritable bowel syndrome.

Indexed as

AcetylationAmino AcidsAnimalsChromatin ImmunoprecipitationFemaleHistone Deacetylase InhibitorsHistonesHydroxamic AcidsHyperalgesiaRats, Sprague-DawleyReceptors, Metabotropic GlutamateReceptors, N-Methyl-D-AspartateRNA, MessengerSpinal CordStress, PsychologicalVisceraAmino AcidsHistone Deacetylase InhibitorsHistonesHydroxamic AcidsLY 341495metabotropic glutamate receptor 2metabotropic glutamate receptor 3Receptors, Metabotropic GlutamateReceptors, N-Methyl-D-AspartateRNA, MessengerVorinostatXanthenes

Identifiers

PMID27385724
PMCPMC4956148
OpenAlexW2463503085

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.