Evidence map›Paper›PMID 17266762›Full record

ArticleGenome biology2007

Differential gene expression patterns in cyclooxygenase-1 and cyclooxygenase-2 deficient mouse brain.

Christopher D Toscano, Vinaykumar V Prabhu, Robert Langenbach, Kevin G Becker, Francesca Bosetti

Open access · goldAbstract read
In one paragraph

Article in Genome biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Are cyclooxygenase-2 and nitric oxide involved in the dyskinesia of Parkinson's disease induced by L-DOPA?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Cyclooxygenases and 5-lipoxygenase in Alzheimer's disease.Progress in neuro-psychopharmacology & biological psychiatry · 2011
    Review
  12. Cyclooxygenase-1 and -2 differentially modulate lipopolysaccharide-induced blood-brain barrier disruption through matrix metalloproteinase activity.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2010
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

5 authors at 3 institutions in 1 country.

Christopher D ToscanoBrain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA. toscanoc@mail.nih.gov
Vinaykumar V Prabhu
Robert Langenbach
Kevin G Becker
Francesca Bosetti
National Institutes of Health · USNational Institute of Environmental Health Sciences · USNational Institute on Aging · US

Funding

Role of cyclooxygenases in excitotoxic brain injuryZ01AG000427 · NIA · NATIONAL INSTITUTE ON AGING · PI BOSETTI, FRANCESCA · 2007 to 2008
$421k
Study of brain arachidonic acid metabolism using knockout miceZ01AG000423 · NIA · AGING · PI BOSETTI, FRANCESCA · 2004 to 2007
$102k
Intramural NIH HHS
6 · The paper itself

Abstract

backgroundCyclooxygenase (COX)-1 and COX-2 produce prostanoids from arachidonic acid and are thought to have important yet distinct roles in normal brain function. Deletion of COX-1 or COX-2 results in profound differences both in brain levels of prostaglandin E2 and in activation of the transcription factor nuclear factor-kappaB, suggesting that COX-1 and COX-2 play distinct roles in brain arachidonic acid metabolism and regulation of gene expression. To further elucidate the role of COX isoforms in the regulation of the brain transcriptome, microarray analysis of gene expression in the cerebral cortex and hippocampus of mice deficient in COX-1 (COX-1-/-) or COX-2 (COX-2-/-) was performed.

resultsA majority (>93%) of the differentially expressed genes in both the cortex and hippocampus were altered in one COX isoform knockout mouse but not the other. The major gene function affected in all genotype comparisons was 'transcriptional regulation'. Distinct biologic and metabolic pathways that were altered in COX-/- mice included beta oxidation, methionine metabolism, janus kinase signaling, and GABAergic neurotransmission.

conclusionOur findings suggest that COX-1 and COX-2 differentially modulate brain gene expression. Because certain anti-inflammatory and analgesic treatments are based on inhibition of COX activity, the specific alterations observed in this study further our understanding of the relationship of COX-1 and COX-2 with signaling pathways in brain and of the therapeutic and toxicologic consequences of COX inhibition.

Indexed as

Gene Expression ProfilingAnimalsCerebral CortexCyclooxygenase 1Cyclooxygenase 2GABA Plasma Membrane Transport ProteinsGene Expression RegulationGenotypeHippocampusJanus KinasesMethionineMiceMice, KnockoutOxidation-ReductionReceptors, GABAUp-RegulationCyclooxygenase 1Cyclooxygenase 2GABA Plasma Membrane Transport ProteinsJanus KinasesMethionineReceptors, GABA

Identifiers

PMID17266762
PMCPMC1839133
OpenAlexW2159383211

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.