Evidence map›Paper›PMID 35655748›Full record

ArticleFrontiers in pain research (Lausanne, Switzerland)2022

Early and Late Transcriptional Changes in Blood, Neural, and Colon Tissues in Rat Models of Stress-Induced and Comorbid Pain Hypersensitivity Reveal Regulatory Roles in Neurological Disease.

Evelina Mocci, Taichi Goto, Jie Chen, Seth Ament, Richard J Traub, Susan G Dorsey

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pain research (Lausanne, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 56% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

6 authors at 1 institution in 1 country.

Evelina MocciDepartment of Pain and Translational Symptom Science, University of Maryland School of Nursing, University of Maryland Baltimore, Baltimore, MD, United States.
Taichi GotoDepartment of Pain and Translational Symptom Science, University of Maryland School of Nursing, University of Maryland Baltimore, Baltimore, MD, United States.
Jie ChenDepartment of Pain and Translational Symptom Science, University of Maryland School of Nursing, University of Maryland Baltimore, Baltimore, MD, United States.
Seth AmentInstitute for Genome Sciences, University of Maryland School of Medicine, University of Maryland Baltimore, Baltimore, MD, United States.
Richard J TraubDepartment of Neural and Pain Sciences, University of Maryland School of Dentistry, University of Maryland Baltimore, Baltimore, MD, United States.
Susan G DorseyDepartment of Pain and Translational Symptom Science, University of Maryland School of Nursing, University of Maryland Baltimore, Baltimore, MD, United States.
University of Maryland, Baltimore · US

Funding

Mechanisms Underlying Comorbid Pain Conditions in a Clinically Relevant ModelR01NR015472 · NINR · UNIVERSITY OF MARYLAND BALTIMORE · PI DORSEY, SUSAN G, TRAUB, RICHARD J · 2015 to 2019
$3.0M
NINR NIH HHS R01 NR015472
6 · The paper itself

Abstract

Background: Irritable bowel syndrome (IBS) and temporomandibular disorder (TMD) are two chronic pain conditions that frequently overlap in the same individual, more commonly in women. Stress is a significant risk factor, exacerbating or triggering one or both conditions. However, the mechanisms underlying IBS-TMD co-morbidity are mostly unknown. Aim: To detect both specific and common stress-induced visceral hypersensitivity (SIH) and comorbid TMD-IBS pain hypersensitivity (CPH) genetic signatures over time. Method: Twenty-four female rats were randomly assigned to one of three experimental groups: naïve, SIH, and CPH (orofacial pain plus stress). RNA was extracted from blood, colon, spinal cord, and dorsal root ganglion 1 or 7 weeks after the stress paradigm. We combined differential gene expression and co-expression network analyses to define both SIH and CPH expression profiles across tissues and time. Results: The transcriptomic profile in blood and colon showed increased expression of genes enriched in inflammatory and neurological biological processes in CPH compared to SIH rats, both at 1 and 7 weeks after stress. In lumbosacral spinal tissue, both SIH and CPH rats compared to naïve revealed decreased expression of genes related to synaptic activity and increased expression of genes enriched in "angiogenesis," "Neurotrophin," and "PI3K-Akt" pathways. Compared to SIH, CPH rats showed increased expression of angiogenesis-related genes 1 week after exposure to stress, while 7 weeks post-stress the expression of these genes was higher in SIH rats. In dorsal root ganglia (DRG), CPH rats showed decreased expression of immune response genes at week 1 and inhibition of nerve myelination genes at 7 weeks compared to naïve. For all tissues, we observed higher expression of genes involved in ATP production in SIH compared to CPH at 1 week and this was reversed 7 weeks after the induction of stress. Conclusion: Our study highlights an increased inflammatory response in CPH compared to SIH rats in the blood and colon. DRG and spinal transcriptomic profiles of both CPH and SIH rats showed inhibition of synaptic activity along with activation of angiogenesis. Targeting these biological processes may lead to a more profound understanding of the mechanisms underlying IBS-TMD comorbidities and new diagnostic and therapeutic strategies.

Indexed as

bloodchronic overlapping pain conditionscolonDRGRNA seqspinalstressWGCNA

Identifiers

PMID35655748
PMCPMC9152010
OpenAlexW4280645268

What Socratic holds

Textmetadata
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 Socratic graph.