Evidence map›Paper›PMID 20454616›Full record

ArticlePloS one2010

Role of PAF receptor in proinflammatory cytokine expression in the dorsal root ganglion and tactile allodynia in a rodent model of neuropathic pain.

Shigeo Hasegawa, Yuta Kohro, Miho Shiratori, Satoshi Ishii, Takao Shimizu, Makoto Tsuda, Kazuhide Inoue

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. The Role of ATP Receptors in Pain Signaling.Neurochemical research · 2022
    Review
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  11. Relief from neuropathic pain by blocking of the platelet-activating factor-pain loop.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  12. Article
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  15. Activation of platelet-activating factor receptor exacerbates renal inflammation and promotes fibrosis.Laboratory investigation; a journal of technical methods and pathology · 2014
    Article
  16. Article
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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

7 authors at 2 institutions in 1 country.

Shigeo HasegawaDepartment of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Yuta Kohro
Miho Shiratori
Satoshi Ishii
Takao Shimizu
Makoto Tsuda
Kazuhide Inoue
Kyushu University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuropathic pain is a highly debilitating chronic pain following damage to peripheral sensory neurons and is often resistant to all treatments currently available, including opioids. We have previously shown that peripheral nerve injury induces activation of cytosolic phospholipase A(2) (cPLA(2)) in injured dorsal root ganglion (DRG) neurons that contribute to tactile allodynia, a hallmark of neuropathic pain. However, lipid mediators downstream of cPLA(2) activation to produce tactile allodynia remain to be determined. PRINCIPAL

findingsHere we provide evidence that platelet-activating factor (PAF) is a potential candidate. Pharmacological blockade of PAF receptors (PAFRs) reduced the development and expression of tactile allodynia following nerve injury. The expression of PAFR mRNA was increased in the DRG ipsilateral to nerve injury, which was seen mainly in macrophages. Furthermore, mice lacking PAFRs showed a reduction of nerve injury-induced tactile allodynia and, interestingly, a marked suppression of upregulation of tumor necrosis factor alpha (TNFalpha) and interleukin-1beta (IL-1beta) expression in the injured DRG, crucial proinflammatory cytokines involved in pain hypersensitivity. Conversely, a single injection of PAF near the DRG of naïve rats caused a decrease in the paw withdrawal threshold to mechanical stimulation in a dose-dependent manner and an increase in the expression of mRNAs for TNFalpha and IL-1beta, both of which were inhibited by pretreatment with a PAFR antagonist.

conclusionsOur results indicate that the PAF/PAFR system has an important role in production of TNFalpha and IL-1beta in the DRG and tactile allodynia following peripheral nerve injury and suggest that blocking PAFRs may be a viable therapeutic strategy for treating neuropathic pain.

Indexed as

Touch1-Acylglycerol-3-Phosphate O-AcyltransferaseAnimalsCyclooxygenase InhibitorsDisease Models, AnimalGanglia, SpinalInflammation MediatorsInjectionsInterleukin-1betaLipoxygenase InhibitorsMiceModels, BiologicalPainPeripheral Nerve InjuriesPeripheral NervesPlatelet Activating Factor1-Acylglycerol-3-Phosphate O-AcyltransferaseCyclooxygenase InhibitorsInflammation MediatorsInterleukin-1betaLipoxygenase InhibitorsPlatelet Activating Factorplatelet activating factor receptorPlatelet Membrane GlycoproteinsReceptors, G-Protein-CoupledReceptors, Lysophosphatidic AcidTumor Necrosis Factor-alpha

Identifiers

PMID20454616
PMCPMC2862737
OpenAlexW1994561593

What OpenQuestion 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 OpenQuestion graph.