Evidence map›Paper›PMID 20152050›Full record

ArticleMolecular pain2010

Kinin B1 receptors contributes to acute pain following minor surgery in humans.

May Hamza, Xiao-Min Wang, Albert Adam, Jaime S Brahim, Janet S Rowan, Gilberto N Carmona, Raymond A Dionne

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Mechanisms for Reducing Neuropathic Pain.Molecular neurobiology · 2020
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Orofacial pain.Pain · 2011
    Review
  14. 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

7 authors at 4 institutions in 3 countries.

May HamzaNINR/NIH, 10 Center drive, Bethesda, MD 20892, USA.
Xiao-Min Wang
Albert Adam
Jaime S Brahim
Janet S Rowan
Gilberto N Carmona
Raymond A Dionne
National Institutes of Health · USNational Institute of Dental and Craniofacial Research · USCardinal Glennon Children’s Medical Center · USUniversité de Montréal · CA

Funding

Molecular-Genetic Mechs Underlying Effects of Anti-inflammatory/Analgesic DrugsZIANR000014 · NINR · NATIONAL INSTITUTE OF NURSING RESEARCH · PI CASHION, ANN · 2009 to 2013
$7.5M
Experimental Therapeutics for Chronic Pain and Symptoms ManagementZIANR000013 · NINR · NATIONAL INSTITUTE OF NURSING RESEARCH · PI SALIGAN, LEOREY · 2009 to 2012
$2.1M
6 · The paper itself

Abstract

backgroundKinins play an important role in regulation of pain and hyperalgesia after tissue injury and inflammation by activating two types of G-protein-coupled receptors, the kinin B1 and B2 receptors. It is generally accepted that the B2 receptor is constitutively expressed, whereas the B1 receptor is induced in response to inflammation. However, little is known about the regulatory effects of kinin receptors on the onset of acute inflammation and inflammatory pain in humans. The present study investigated the changes in gene expression of kinin receptors and the levels of their endogenous ligands at an early time point following tissue injury and their relation to clinical pain, as well as the effect of COX-inhibition on their expression levels.

resultsTissue injury resulted in a significant up-regulation in the gene expression of B1 and B2 receptors at 3 hours post-surgery, the onset of acute inflammatory pain. Interestingly, the up-regulation in the gene expression of B1 and B2 receptors was positively correlated to pain intensity only after ketorolac treatment, signifying an interaction between prostaglandins and kinins in the inflammatory pain process. Further, the gene expression of both B1 and B2 receptors were correlated. Following tissue injury, B1 ligands des-Arg9-BK and des-Arg10-KD were significantly lower at the third hour compared to the first 2 hours in both the placebo and the ketorolac treatment groups but did not differ significantly between groups. Tissue injury also resulted in the down-regulation of TRPV1 gene expression at 3 hours post-surgery with no significant effect by ketorolac treatment. Interestingly, the change in gene expression of TRPV1 was correlated to the change in gene expression of B1 receptor but not B2 receptor.

conclusionsThese results provide evidence at the transcriptional level in a clinical model of tissue injury that up-regulation of kinin receptors are involved in the development of the early phase of inflammation and inflammatory pain. The up-regulation of B1 receptors may contribute to acute inflammatory pain through TRPV1 activation.

Indexed as

Acute DiseaseAdolescentAdultBradykininCyclooxygenase InhibitorsDown-RegulationFemaleGene Expression RegulationHumansInflammationKetorolacMalePostoperative PainReceptor, Bradykinin B1Receptor, Bradykinin B2RNA, MessengerBradykininCyclooxygenase InhibitorsKetorolacReceptor, Bradykinin B1Receptor, Bradykinin B2RNA, MessengerTRPV1 protein, humanTRPV Cation Channels

Identifiers

PMID20152050
PMCPMC2834653
OpenAlexW2107152434

What OpenQuestion holds

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Registered trials

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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.