Evidence map›Paper›PMID 33244261›Full record

ArticleJournal of pain research2020

DNA Microarray Analysis of Differential Gene Expression in the Dorsal Root Ganglia of Four Different Neuropathic Pain Mouse Models.

Hiroyuki Yokoyama, Takashi Hirai, Tetsuya Nagata, Mitsuhiro Enomoto, Hidetoshi Kaburagi, Li Leiyo, Takayuki Motoyoshi, Toshitaka Yoshii, Atsushi Okawa, Takanori Yokota

Open access · goldAbstract read
In one paragraph

Article in Journal of pain research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Sigma-1 Receptors Control Neuropathic Pain and Peripheral Neuroinflammation After Nerve Injury in Female Mice: A Transcriptomic Study.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    Article
  5. Article
  6. Article
  7. Transcriptomic and proteomic profiling of NaFrontiers in molecular neuroscience · 2022
    Article
  8. 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

10 authors at 1 institution in 1 country.

Hiroyuki YokoyamaDepartment of Orthopedic Surgery, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
Takashi HiraiDepartment of Orthopedic Surgery, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.ORCID 0000-0001-6200-0100
Tetsuya NagataDepartment of Neurology and Neurological Science, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
Mitsuhiro EnomotoDepartment of Orthopedic Surgery, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
Hidetoshi KaburagiDepartment of Orthopedic Surgery, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.ORCID 0000-0003-4272-6347
Li LeiyoDepartment of Orthopedic Surgery, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
Takayuki MotoyoshiDepartment of Orthopedic Surgery, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
Toshitaka YoshiiDepartment of Orthopedic Surgery, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
Atsushi OkawaDepartment of Orthopedic Surgery, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
Takanori YokotaDepartment of Neurology and Neurological Science, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
Tokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposePathological stimuli or injury to the peripheral nervous system can trigger neuropathic pain with common clinical features such as allodynia and hypersensitivity. Although various studies have identified molecules or genes related to neuropathic pain, the essential components are still unclear. Therefore, in this study, we investigated the molecular and genetic factors related to neuropathic pain.

methodsWe extracted candidate genes in the dorsal root ganglion (DRG) from three nerve injury mouse models and a sham-operated model (sciatic nerve ligation and resection, sural nerve resection, spared nerve injury [SNI], and sham) using DNA microarray to elucidate the genes responsible for the neuropathic pain mechanism in the SNI model, which exhibits hypersensitivity in the hindpaw of the preserved sural nerve area. We eliminated as many biases as possible. We then focused on an upregulated endogenous vasopressin receptor and clarified whether it is closely associated with traumatic neuropathic pain using a knockout mouse and drug-mediated suppression of the gene.

resultsAlgorithm analysis of DNA microarray results identified 50 genes significantly upregulated in the DRG of the SNI model. Two independent genes-cyclin-dependent kinase-1 (CDK-1) and arginine vasopressin receptor 1A (V1a)-were subsequently identified as candidate SNI-specific genes in the DRG by quantitative PCR analysis. Administration of V1a agonist to wild-type SNI mice significantly alleviated neuropathic pain. However, V1a knockout mice did not exhibit higher hypersensitivity to mechanical stimulation than wild-type mice. In addition, V1a knockout mice showed similar pain behaviors after SNI to wild-type mice.

conclusionThrough the DNA microarray analysis of several neuropathic models, we detected specific genes related to chronic pain. In particular, our results suggest that V1a in the DRG may partially contribute to the mechanism of neuropathic pain.

Indexed as

arginine vasopressin 1adorsal root ganglionmicroarraymolecular targetneuropathic painperipheral nerve injury

Identifiers

PMID33244261
PMCPMC7685567
OpenAlexW3105878354

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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.