Evidence map›Paper›PMID 25147926›Full record

ArticlePloS one2014

Cellular adhesion gene SELP is associated with rheumatoid arthritis and displays differential allelic expression.

Jana Burkhardt, Mechthild Blume, Elisabeth Petit-Teixeira, Vitor Hugo Teixeira, Anke Steiner, Elfi Quente, Grit Wolfram, Markus Scholz, Céline Pierlot, Paola Migliorini and 12 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-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

15 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Association of the rs3917647 polymorphism of the SELP gene with malnutrition in gastric cancer.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2023
    Article
  4. The roles of P-selectin in cancer cachexia.Medical oncology (Northwood, London, England) · 2023
    Review
  5. Article
  6. The impact ofSaudi journal of biological sciences · 2023
    Article
  7. Article
  8. TheJournal of inflammation research · 2023
    Article
  9. Article
  10. Article
  11. 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

22 authors at 12 institutions in 8 countries.

Jana BurkhardtTranslational Centre for Regenerative Medicine (TRM), Universität Leipzig, Leipzig, Germany.
Mechthild BlumeUniversity Leipzig, Institute for Clinical Immunology and Tranfusion Medicine (IKIT), Universität Leipzig, Leipzig, Germany.
Elisabeth Petit-TeixeiraGenhotel-EA 3886, Université d'Evry-Val d'Essonne, Evry, France.
Vitor Hugo TeixeiraCentre for Respiratory Research, University College London, London, United Kingdom.
Anke SteinerUniversity Leipzig, Institute for Clinical Immunology and Tranfusion Medicine (IKIT), Universität Leipzig, Leipzig, Germany.
Elfi QuenteFraunhofer Institute for Celltherapy and Immunology (IZI), Leipzig, Germany.
Grit WolframTranslational Centre for Regenerative Medicine (TRM), Universität Leipzig, Leipzig, Germany.
Markus ScholzLIFE - Leipzig Research Center for Civilization Diseases, Universität Leipzig, Leipzig, Germany.
Céline PierlotGenhotel-EA 3886, Université d'Evry-Val d'Essonne, Evry, France.
Paola MiglioriniPisa University, Pisa, Italy.
Stefano BombardieriPisa University, Pisa, Italy.
Alejandro BalsaLa Paz Hospital, Madrid, Spain.
René WesthovensRheumatology KU Leuven, Leuven, Belgium.
Pilar BarreraNijmegen University, Nijmegen, the Netherlands.
Timothy R D J RadstakeUniversity Medical Center Utrecht, Utrecht, the Netherlands.
Helena AlvesPorto San Joao Hospital, Porto, Portugal.
Thomas BardinFédération de Rhumatologie, Lariboisière Hospital, Paris, France.
Bernard PrumLaboratoire Statistique & Génome, Université d'Evry-Val d'Essonne, Evry, France.
Frank EmmrichTranslational Centre for Regenerative Medicine (TRM), Universität Leipzig, Leipzig, Germany; University Leipzig, Institute for Clinical Immunology and Tranfusion Medicine (IKIT), Universität Leipzig, Leipzig, Germany; Fraunhofer Institute for Celltherapy and Immunology (IZI), Leipzig, Germany.
François CornelisGenHotel-Auvergne, Université d'Auvergne, Clermont-Ferrand, France.
Peter AhnertLIFE - Leipzig Research Center for Civilization Diseases, Universität Leipzig, Leipzig, Germany; Institute for Medical Informatics, Statistics and Epidemiology (IMISE), Universität Leipzig, Leipzig, Germany.
Holger KirstenFraunhofer Institute for Celltherapy and Immunology (IZI), Leipzig, Germany; LIFE - Leipzig Research Center for Civilization Diseases, Universität Leipzig, Leipzig, Germany; Institute for Medical Informatics, Statistics and Epidemiology (IMISE), Universität Leipzig, Leipzig, Germany.
Leipzig University · DEUniversité d'Évry Val-d'Essonne · FRFraunhofer Institute for Cell Therapy and Immunology · DEUniversity of Pisa · ITHôpital Lariboisière · FRHospital de São João · PTHospital Universitario La Paz · ESKU Leuven · BERadboud University Nijmegen · NLUniversité Clermont Auvergne · FRUniversity College London · GBUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In rheumatoid arthritis (RA), a key event is infiltration of inflammatory immune cells into the synovial lining, possibly aggravated by dysregulation of cellular adhesion molecules. Therefore, single nucleotide polymorphisms of 14 genes involved in cellular adhesion processes (CAST, ITGA4, ITGB1, ITGB2, PECAM1, PTEN, PTPN11, PTPRC, PXN, SELE, SELP, SRC, TYK2, and VCAM1) were analyzed for association with RA. Association analysis was performed consecutively in three European RA family sample groups (Nfamilies = 407). Additionally, we investigated differential allelic expression, a possible functional consequence of genetic variants. SELP (selectin P, CD62P) SNP-allele rs6136-T was associated with risk for RA in two RA family sample groups as well as in global analysis of all three groups (ptotal = 0.003). This allele was also expressed preferentially (p<10-6) with a two- fold average increase in regulated samples. Differential expression is supported by data from Genevar MuTHER (p1 = 0.004; p2 = 0.0177). Evidence for influence of rs6136 on transcription factor binding was also found in silico and in public datasets reporting in vitro data. In summary, we found SELP rs6136-T to be associated with RA and with increased expression of SELP mRNA. SELP is located on the surface of endothelial cells and crucial for recruitment, adhesion, and migration of inflammatory cells into the joint. Genetically determined increased SELP expression levels might thus be a novel additional risk factor for RA.

Indexed as

AllelesGene Expression RegulationAdultAge of OnsetArthritis, RheumatoidBinding SitesCell AdhesionComputational BiologyDatabases, GeneticFemaleGenetic Association StudiesGenotypeHumansMalePolymorphism, Single NucleotideProtein BindingP-SelectinSELP protein, humanTranscription Factors

Identifiers

PMID25147926
PMCPMC4141704
OpenAlexW2140681886

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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.