Evidence map›Paper›PMID 18721452›Full record

ArticleArthritis research & therapy2008

Identification of intra-group, inter-individual, and gene-specific variances in mRNA expression profiles in the rheumatoid arthritis synovial membrane.

René Huber, Christian Hummert, Ulrike Gausmann, Dirk Pohlers, Dirk Koczan, Reinhard Guthke, Raimund W Kinne

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

73 citing papers in PubMed, 107 citations in OpenAlex.

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13 more citing papers are in PubMed but not listed here.

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 1 country.

René HuberDepartment of Orthopedics, Experimental Rheumatology Unit, University Hospital Jena, Waldkrankenhaus Rudolf Elle, Eisenberg, Germany.
Christian Hummert
Ulrike Gausmann
Dirk Pohlers
Dirk Koczan
Reinhard Guthke
Raimund W Kinne
Waldkrankenhaus Rudolf Elle · DELeibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEUniversity of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionRheumatoid arthritis (RA) is a chronic inflammatory and destructive joint disease characterized by overexpression of pro-inflammatory/pro-destructive genes and other activating genes (for example, proto-oncogenes) in the synovial membrane (SM). The gene expression in disease is often characterized by significant inter-individual variances via specific synchronization/desynchronization of gene expression. To elucidate the contribution of the variance to the pathogenesis of disease, expression variances were tested in SM samples of RA patients, osteoarthritis (OA) patients, and normal controls (NCs).

methodAnalysis of gene expression in RA, OA, and NC samples was carried out using Affymetrix U133A/B oligonucleotide arrays, and the results were validated by real-time reverse transcription-polymerase chain reaction. For the comparison between RA and NC, 568 genes with significantly different variances in the two groups (P <or= 0.05; Bonferroni/Holm corrected Brown-Forsythe version of the Levene test) were selected. For the comparison between RA and OA, 333 genes were selected. By means of the Kyoto Encyclopedia of Genes and Genomes, the pathways/complexes significantly affected by higher gene expression variances were identified in each group.

resultsTen pathways/complexes significantly affected by higher gene expression variances were identified in RA compared with NC, including cytokine-cytokine receptor interactions, the transforming growth factor-beta pathway, and anti-apoptosis. Compared with OA, three pathways with significantly higher variances were identified in RA (for example, B-cell receptor signaling and vascular endothelial growth factor signaling). Functionally, the majority of the identified pathways are involved in the regulation of inflammation, proliferation, cell survival, and angiogenesis.

conclusionIn RA, a number of disease-relevant or even disease-specific pathways/complexes are characterized by broad intra-group inter-individual expression variances. Thus, RA pathogenesis in different individuals may depend to a lesser extent on common alterations of the expression of specific key genes, and rather on individual-specific alterations of different genes resulting in common disturbances of key pathways.

Indexed as

Gene Expression ProfilingAdultAgedApoptosis Regulatory ProteinsArthritis, RheumatoidCase-Control StudiesCell SurvivalFemaleGenetic VariationHumansInflammationMaleMiddle AgedNeovascularization, PathologicOsteoarthritisReceptors, CytokineApoptosis Regulatory ProteinsReceptors, CytokineRNA, MessengerTransforming Growth Factor betaVascular Endothelial Growth Factor A

Identifiers

PMID18721452
PMCPMC2575612
OpenAlexW2032124256

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LicenceCC BY
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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.