Evidence map›Paper›PMID 17070997›Full record

Trial reportPain2007

Rofecoxib modulates multiple gene expression pathways in a clinical model of acute inflammatory pain.

Xiao-Min Wang, Tian-Xia Wu, May Hamza, Edward S Ramsay, Sharon M Wahl, Raymond A Dionne

Open access · greenAbstract readComparative StudyRandomized Controlled Trial
In one paragraph

Trial report in Pain, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Genomics of pain in osteoarthritis.Osteoarthritis and cartilage · 2013
    Review
  10. Article
  11. Cytokine patterns in brain tumour progression.Mediators of inflammation · 2013
    Article
  12. Article
  13. Article
  14. Genomic methods for clinical and translational pain research.Methods in molecular biology (Clifton, N.J.) · 2012
    Article
  15. Ablation of cyclooxygenase-2 in forebrain neurons is neuroprotective and dampens brain inflammation after status epilepticus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Progress in genetic studies of pain and analgesia.Annual review of pharmacology and toxicology · 2009
    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

6 authors at 2 institutions in 2 countries.

Xiao-Min WangNINR/NIH, Bethesda, MD 20892, USA.
Tian-Xia Wu
May Hamza
Edward S Ramsay
Sharon M Wahl
Raymond A Dionne
National Institutes of Health · USAin Shams University · EG

Funding

Normal/Pathologic Mechanisms Of Inflammation &ImmunityZ01DE000046 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI WAHL, SHARON M · 1985 to 2008
$3.8M
Molecular-Genetic Mechs Underlying Effects of Anti-inflammatory/Analgesic DrugsZ01NR000014 · NINR · NATIONAL INSTITUTE OF NURSING RESEARCH · PI DIONNE, RAYMOND A · 2006 to 2008
$1.8M
Investigations In Infectious And Autoimmune DiseasesZ01DE000691 · NIDCR · DENTAL &CRANIOFACIAL RESEARCH · PI WAHL, SHARON M · 1998 to 2007
$534k
EXPERIMENTAL THERAPEUTICS FOR ACUTE PAINZ01DE000286 · NIDCR · DENTAL &CRANIOFACIAL RESEARCH · PI DIONNE, RAYMOND A · 1985 to 2005
–
Intramural NIH HHSNIDCR NIH HHS Z01 DE000286-26
6 · The paper itself

Abstract

New insights into the biological properties of cyclooxygenase-2 (COX-2) and its response pathway challenge the hypothesis that COX-2 is simply pro-inflammatory and inhibition of COX-2 solely prevents the development of inflammation and ameliorates inflammatory pain. The present study performed a comprehensive analysis of gene/protein expression induced by a selective inhibitor of COX-2, rofecoxib, compared with a non-selective COX inhibitor, ibuprofen, and placebo in a clinical model of acute inflammatory pain (the surgical extraction of impacted third molars) using microarray analysis followed by quantitative RT-PCR verification and Western blotting. Inhibition of COX-2 modulated gene expression related to inflammation and pain, the arachidonic acid pathway, apoptosis/angiogenesis, cell adhesion and signal transduction. Compared to placebo, rofecoxib treatment increased the gene expression of ANXA3 (annexin 3), SOD2 (superoxide dismutase 2), SOCS3 (suppressor of cytokine signaling 3) and IL1RN (IL1 receptor antagonist) which are associated with inhibition of phospholipase A(2) and suppression of cytokine signaling cascades, respectively. Both rofecoxib and ibuprofen treatment increased the gene expression of the pro-inflammatory mediators, IL6 and CCL2 (chemokine C-C motif ligand 2), following tissue injury compared to the placebo treatment. These results indicate a complex role for COX-2 in the inflammatory cascade in addition to the well-characterized COX-dependent pathway, as multiple pathways are also involved in rofecoxib-induced anti-inflammatory and analgesic effects at the gene expression level. These findings may also suggest an alternative hypothesis for the adverse effects attributed to selective inhibition of COX-2.

Indexed as

Acute DiseaseAdolescentAdultAnti-Inflammatory AgentsCyclooxygenase 2 InhibitorsCytokinesFemaleGene ExpressionGene Expression RegulationHumansIbuprofenImmunologic FactorsInflammationLactonesMalePainAnti-Inflammatory AgentsCyclooxygenase 2 InhibitorsCytokinesIbuprofenImmunologic FactorsLactonesrofecoxibSulfones

Identifiers

PMID17070997
PMCPMC1894940
OpenAlexW2019004042

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.