Evidence map›Paper›PMID 16955275›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2006

Short-term hyperthermia prevents activation of proinflammatory genes in fibroblast-like synoviocytes by blocking the activation of the transcription factor NF-kappaB.

Marica Markovic, Karl M Stuhlmeier

Abstract read
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In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. It is time to thoroughly study the effects of mild stress in rodents, but also in human beings.Dose-response : a publication of International Hormesis Society · 2009
    Article
  5. Article
  6. Article
  7. On Fever, famine, and war--but mostly fever.Journal of molecular medicine (Berlin, Germany) · 2006
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution.

Marica MarkovicInstitute of Medical Biochemistry, Clinical Center of Serbia, Belgrade, Serbia.
Karl M Stuhlmeier
Ludwig Boltzmann Institute for Digital Health and Prevention

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast-like synoviocytes (FLS) play a key role in the genesis of rheumatoid arthritis (RA). FLS are among the most versatile cells with the potential to activate an array of genes that are able to initiate and propagate inflammation in RA-affected joints. Controlling activation of FLS might hold the key to restraining inflammation in RA-affected joints. In this study, we investigate the effect and mechanisms of short-term hyperthermia on a series of proinflammatory genes in FLS. In vitro experiments demonstrate that exposure of FLS to elevated temperatures for the duration of 30 min prevents activation of a series of genes with proinflammatory properties. Exposure to hyperthermia reduces IL-1beta-induced prostaglandin E2 release, suppresses activation of the adhesion molecules VCAM-1, ICAM-1, the cytokines TNFalpha, IL-1alpha, IL-1beta, IL-8 as well as COX-2 protein synthesis. Real time reverse transcriptase-polymerase chain reaction showed that hyperthermia altered gene expression at the transcriptional level. The amount and the duration of inhibition is gene-specific and lasts for up to 25 h. As to the mechanism of inhibition, electrophoretic mobility shift assay experiments demonstrated that exposure of FLS to hyperthermia prevents IL-1beta-induced NF-kappaB translocation and subsequent DNA binding. Many mechanisms have been shown to be involved in hyperthermia-mediated effects on NF-kappaB-DNA interactions. We demonstrate by Western blot experiments that in FLS, hyperthermia prevents the phosphorylation and subsequent degradation of IkappaBalpha, therefore retaining the NF-kappaB complex in the cytoplasm. Carefully controlled in vivo tests are certainly needed before one can take full advantage of those phenomena; however, the ease by which the temperature in joints can be modulated might offer an opportunity for manipulating inflammatory processes in joints by simple balneological means.

Indexed as

TemperatureArthritis, RheumatoidBlotting, WesternCells, CulturedCyclooxygenase 2DinoprostoneElectrophoretic Mobility Shift AssayFibroblastsGene Expression RegulationHeme Oxygenase-1HSP70 Heat-Shock ProteinsHumansI-kappa B ProteinsIntercellular Adhesion Molecule-1Interleukin-1betaMembrane ProteinsCyclooxygenase 2DinoprostoneHeme Oxygenase-1HMOX1 protein, humanHSP70 Heat-Shock ProteinsI-kappa B ProteinsIntercellular Adhesion Molecule-1Interleukin-1betaMembrane ProteinsNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanPTGS2 protein, human

Identifiers

PMID16955275
OpenAlexW2121282546

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.