Evidence map›Paper›PMID 17310141›Full record

ArticleBritish journal of pharmacology2007

Intraplantar PGE2 causes nociceptive behaviour and mechanical allodynia: the role of prostanoid E receptors and protein kinases.

C A L Kassuya, J Ferreira, R F Claudino, J B Calixto

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In one paragraph

Article in British journal of pharmacology, 2007. 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
2.7field-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

20 citing papers in PubMed, 90 citations in OpenAlex.

  1. Trial
  2. Article
  3. PGE2 Potentiates Orai1-Mediated Calcium Entry Contributing to Peripheral Sensitization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  4. Stem cells and pain.World journal of stem cells · 2023
    Review
  5. Article
  6. Article
  7. Injury-Induced Effectors of Neuropathic Pain.Molecular neurobiology · 2020
    Review
  8. Article
  9. Antinociceptive Activities of the Methanolic Extract of the Stem Bark ofEvidence-based complementary and alternative medicine : eCAM · 2017
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Molecular Roles of Cdk5 in Pain Signaling.Drug discovery today. Therapeutic strategies · 2009
    Article
  20. 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

4 authors at 2 institutions in 1 country.

C A L KassuyaDepartment of Pharmacology, Universidade Federal de Santa Catarina, Florianópolis, Santa Catarina, Brazil.
J Ferreira
R F Claudino
J B Calixto
Universidade Federal de Santa Catarina · BRUniversidade Federal de Santa Maria · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeReceptor subtypes involved in PGE(2)-induced nociception are still controversial. The present study investigated the prostanoid E receptor (EP) subtypes and the protein kinase (PK) pathways involved in the nociception induced by PGE(2) injection in the mouse paw. EXPERIMENTAL APPROACH: Paw-licking and mechanical allodynia were measured in vivo and protein kinase activation ex vivo by Western blots of extracts of paw skin. KEY

resultsIntraplantar (i.pl.) injection of PGE(2) into the mouse paw caused nociceptive behaviour of short duration with mean ED(50) of 1.43 nmol. PGE(2) produced a longer-lasting mechanical allodynia, with an ED(50) of 0.05 nmol. Intraplantar injection of antagonists at EP(3) or EP(4), but not at EP(1) or EP(2) receptors inhibited PGE(2)-induced paw-licking. Paw-licking caused by PGE(2) was blocked by an inhibitor of PKA but only partially decreased by inhibition of the extracellular-regulated kinase (ERK). Selective inhibitors of PKC, c-Jun N-terminal kinase (JNK) or p38, all failed to affect PGE(2)-induced paw-licking. An EP(3) antagonist inhibited PGE(2)-induced mechanical allodynia. However, inhibitors of PKA, PKC or ERK, but not p38 or JNK, also partially inhibited PGE(2)-induced mechanical allodynia. Western blot analyses confirmed that i.pl. injection of PGE(2) activated PKA, PKCalpha, and mitogen activated kinases (MAPKs) in the paw. Co-treatment with EP(3) or EP(4) receptor antagonists reduced PGE(2)-induced PKA and ERK, but not PKCalpha activation. CONCLUSIONS AND IMPLICATIONS: The present results indicate that the nociceptive behaviour and mechanical allodynia caused by i.pl. PGE(2) are mediated through activation of distinct EP receptors and PK-dependent mechanisms.

Indexed as

AcrylamidesAnimalsCarrageenanCyclic AMP-Dependent Protein KinasesDinoprostoneExtracellular Signal-Regulated MAP KinasesIn Vitro TechniquesMaleMiceNaphthalenesNociceptorsPain MeasurementProstaglandins E, SyntheticProtein Kinase CProtein KinasesReceptors, Prostaglandin E17-phenyltrinorprostaglandin E2AcrylamidesCarrageenanCyclic AMP-Dependent Protein KinasesDinoprostoneExtracellular Signal-Regulated MAP KinasesL-826266NaphthalenesProstaglandins E, SyntheticProtein Kinase CProtein KinasesReceptors, Prostaglandin E

Identifiers

PMID17310141
PMCPMC2013868
OpenAlexW2058371150

What OpenQuestion holds

Textmetadata
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.