Evidence map›Paper›PMID 27702909›Full record

ArticleMolecular pain2016

Transcriptome analysis of trigeminal ganglia following masseter muscle inflammation in rats.

Man-Kyo Chung, Jennifer Park, Jamila Asgar, Jin Y Ro

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 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

42 citing papers in PubMed, 57 citations in OpenAlex.

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  3. CD4Proceedings 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

4 authors at 1 institution in 1 country.

Man-Kyo ChungDepartment of Neural and Pain Sciences, Center to Advance Chronic Pain Research, University of Maryland Dental School, Baltimore, MD, USA mchung@umaryland.edu.
Jennifer ParkDepartment of Neural and Pain Sciences, Center to Advance Chronic Pain Research, University of Maryland Dental School, Baltimore, MD, USA.
Jamila AsgarDepartment of Neural and Pain Sciences, Center to Advance Chronic Pain Research, University of Maryland Dental School, Baltimore, MD, USA.
Jin Y RoDepartment of Neural and Pain Sciences, Center to Advance Chronic Pain Research, University of Maryland Dental School, Baltimore, MD, USA.
University of Maryland, Baltimore · US

Funding

Peripheral Receptor Mechanisms in Orofacial Muscle PainR01DE016062 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI RO, JIN Y · 2005 to 2022
$5.6M
Genetic and post-translational modifications of TRPV1 in craniofacial painR01DE023846 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI CHUNG, MAN-KYO · 2014 to 2018
$1.9M
NIDCR NIH HHS R01 DE016062NIDCR NIH HHS R01 DE023846
6 · The paper itself

Abstract

backgroundChronic pain in masticatory muscles is a major medical problem. Although mechanisms underlying persistent pain in masticatory muscles are not fully understood, sensitization of nociceptive primary afferents following muscle inflammation or injury contributes to muscle hyperalgesia. It is well known that craniofacial muscle injury or inflammation induces regulation of multiple genes in trigeminal ganglia, which is associated with muscle hyperalgesia. However, overall transcriptional profiles within trigeminal ganglia following masseter inflammation have not yet been determined. In the present study, we performed RNA sequencing assay in rat trigeminal ganglia to identify transcriptome profiles of genes relevant to hyperalgesia following inflammation of the rat masseter muscle.

resultsMasseter inflammation differentially regulated >3500 genes in trigeminal ganglia. Predominant biological pathways were predicted to be related with activation of resident non-neuronal cells within trigeminal ganglia or recruitment of immune cells. To focus our analysis on the genes more relevant to nociceptors, we selected genes implicated in pain mechanisms, genes enriched in small- to medium-sized sensory neurons, and genes enriched in TRPV1-lineage nociceptors. Among the 2320 candidate genes, 622 genes showed differential expression following masseter inflammation. When the analysis was limited to these candidate genes, pathways related with G protein-coupled signaling and synaptic plasticity were predicted to be enriched. Inspection of individual gene expression changes confirmed the transcriptional changes of multiple nociceptor genes associated with masseter hyperalgesia (e.g., Trpv1, Trpa1, P2rx3, Tac1, and Bdnf) and also suggested a number of novel probable contributors (e.g., Piezo2, Tmem100, and Hdac9).

conclusionThese findings should further advance our understanding of peripheral mechanisms involved in persistent craniofacial muscle pain conditions and provide a rational basis for identifying novel genes or sets of genes that can be potentially targeted for treating such conditions.

Indexed as

AcrylamidesAnimalsBridged Bicyclo Compounds, HeterocyclicFreund's AdjuvantGene Expression ProfilingGene Expression RegulationHyperalgesiaInflammationMaleMasseter MuscleMyalgiaNerve Tissue ProteinsPain ThresholdPrincipal Component AnalysisRatsRats, Sprague-Dawley3-(4-t-butylphenyl)-N-(2,3-dihydrobenzo(b)(1,4)dioxin-6-yl)acrylamideAcrylamidesBridged Bicyclo Compounds, HeterocyclicFreund's AdjuvantNerve Tissue ProteinsRNA, MessengerTRPV1 receptorTRPV Cation ChannelsinflammationMasseter muscleRNA sequencingtranscriptometrigeminal ganglia

Identifiers

PMID27702909
PMCPMC5066585
OpenAlexW2527778140

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.