Evidence map›Paper›PMID 23488692›Full record

ArticleScandinavian journal of immunology2013

IL-1β/HMGB1 complexes promote The PGE2 biosynthesis pathway in synovial fibroblasts.

P Leclerc, H Wähämaa, H Idborg, P J Jakobsson, H E Harris, M Korotkova

Open access · bronzeAbstract read
In one paragraph

Article in Scandinavian journal of immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.2field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
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  8. Observational
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  12. Liquorice for pain?Therapeutic advances in psychopharmacology · 2021
    Review
  13. Article
  14. Selenium and selenoproteins in prostanoid metabolism and immunity.Critical reviews in biochemistry and molecular biology · 2019
    Review
  15. Article
  16. Review
  17. Article
  18. Article
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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 1 institution in 1 country.

P LeclercRheumatology Research Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
H Wähämaa
H Idborg
P J Jakobsson
H E Harris
M Korotkova
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PGE2 is a potent lipid mediator of pain and oedema found elevated in RA. Microsomal prostaglandin E synthase-1 (mPGES-1) is a terminal enzyme of the PGE2 pathway inducible by proinflammatory cytokines. mPGES-1 is markedly upregulated in RA synovial tissue despite antirheumatic treatments, suggesting that multiple inflammatory stimuli contribute to its induction. High-mobility group box chromosomal protein 1 (HMGB1) is known to induce inflammation both by direct interaction with TLR4 and by enhancement of other proinflammatory molecules signalling, through complex formation. The high expression of extracellular HMGB1 within the inflamed synovium, implies its pro-arthritogenic role in RA. We aimed to investigate the effects of IL-1β/HMGB1 complexes on mPGES-1 and other enzymes of the PGE2 pathway in synovial fibroblasts (SFs) from patients with arthritis. Furthermore, we studied the effect of COX-2 inhibition and IL-1RI antagonism on prostanoid and cytokine production by SFs. Stimulation of SFs with HMGB1 in complex with suboptimal amounts of IL-1β significantly increased mPGES-1 and COX-2 expressions as well as PGE2 production, as compared to treatment with HMGB1 or IL-1β alone. Furthermore, NS-398 reduced the production of IL-6 and IL-8, thus indicating that IL-1β/HMGB1 complexes modulate cytokine production in part through prostanoid synthesis. Treatment with IL-1RA completely abolished the induced PGE2 and cytokine production, suggesting an effect mediated through IL-1RI. IL-1β/HMGB1 complexes promote the induction of mPGES-1, COX-2 and PGE2 in SF. The amplification of the PGE2 biosynthesis pathway by HMGB1 might constitute an important pathogenic mechanism perpetuating inflammatory and destructive activities in rheumatoid arthritis.

Indexed as

ArthritisBiosynthetic PathwaysBlotting, WesternCells, CulturedChemokinesCyclooxygenase 2Cyclooxygenase InhibitorsCytokinesDinoprostoneDrug SynergismFibroblastsHMGB1 ProteinHumansInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinInterleukin-6ChemokinesCyclooxygenase 2Cyclooxygenase InhibitorsCytokinesDinoprostoneHMGB1 ProteinInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinInterleukin-6Interleukin-8Intramolecular OxidoreductasesN-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamideNitrobenzenesProstaglandin-E SynthasesPTGES protein, humanPTGS2 protein, humanSulfonamides

Identifiers

PMID23488692
PMCPMC3670302
OpenAlexW2003597161

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.