Evidence map›Paper›PMID 22789984›Full record

ArticleSpine2013

The prostaglandin E2 receptor, EP2, is upregulated in the dorsal root ganglion after painful cervical facet joint injury in the rat.

Jeffrey V Kras, Ling Dong, Beth A Winkelstein

Abstract read
In one paragraph

Article in Spine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. EPScientific reports · 2017
    Article
  8. Article
  9. Article
  10. 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

3 authors at 1 institution in 2 countries.

Jeffrey V KrasDepartment of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104, USA.
Ling Dong
Beth A Winkelstein
Bioengineering Center · RU

Funding

Nociceptive Mechanisms In Whiplash InjuryR01AR056288 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI WINKELSTEIN, BETH A · 2009 to 2013
$1.6M
NIAMS NIH HHS AR056288NIAMS NIH HHS R01 AR056288
6 · The paper itself

Abstract

STUDY

designThis study implemented immunohistochemistry to assay prostaglandin E2 (PGE2) receptor EP2 expression in the dorsal root ganglion (DRG) of rats after painful cervical facet joint injury.

objectiveTo identify if inflammatory cascades are induced in association with cervical facet joint distraction-induced pain by investigating the time course of EP2 expression in the DRG. SUMMARY OF BACKGROUND DATA: The cervical facet joint is a common source of neck pain, and nonphysiological stretch of the facet capsular ligament can initiate pain from the facet joint via mechanical injury. PGE2 levels are elevated in painful inflamed and arthritic joints, and PGE2 sensitizes joint afferents to mechanical stimulation. Although in vitro studies suggest that the EP2 receptor subtype contributes to painful joint disease, the EP2 response has not been investigated for any association with painful mechanical joint injury.

methodsSeparate groups of male Holtzman rats underwent either a painful cervical facet joint distraction injury or sham procedure. Bilateral forepaw mechanical allodynia was assessed, and immunohistochemical techniques were used to quantify EP2 expression in the DRG at days 1 and 7.

resultsFacet joint distraction induced mechanical allodynia that was significant (P < 0.024) at all time points. Painful joint injury also significantly elevated total EP2 expression in the DRG at day 1 (P = 0.009), which was maintained at day 7 (P < 0.001). Neuronal expression of EP2 in the DRG was only increased over sham levels at day 1 (P = 0.013).

conclusionPainful cervical facet joint distraction induces an immediate and sustained increase of EP2 expression in the DRG, implicating peripheral inflammation in the initiation and maintenance of facet joint pain. The transient increase in neuronal EP2 suggests, as in other painful joint conditions, that after joint injury nonneuronal cells may migrate to the DRG, some of which likely express EP2.

Indexed as

AnimalsCervical VertebraeDinoprostoneForelimbGanglia, SpinalHyperalgesiaImmunohistochemistryMalePain MeasurementRatsRats, Sprague-DawleyReceptors, Prostaglandin E, EP2 SubtypeUp-RegulationZygapophyseal JointDinoprostoneReceptors, Prostaglandin E, EP2 Subtype

Identifiers

PMID22789984
PMCPMC3500406
OpenAlexW1969321279

What OpenQuestion holds

Textmetadata
LicenceTDM
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.