Evidence map›Paper›PMID 27863512›Full record

ArticleArthritis research & therapy2016

Rheumatoid synovial fibroblasts differentiate into distinct subsets in the presence of cytokines and cartilage.

Adam P Croft, Amy J Naylor, Jennifer L Marshall, Debbie L Hardie, Birgit Zimmermann, Jason Turner, Guillaume Desanti, Holly Adams, Adrian I Yemm, Ulf Müller-Ladner and 4 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

67 citing papers in PubMed, 100 citations in OpenAlex.

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  9. The Challenges of Local Intra-Articular Therapy.Medicina (Kaunas, Lithuania) · 2024
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7 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

14 authors at 4 institutions in 2 countries.

Adam P CroftRheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham Research Laboratories, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, B15 2WB, UK.
Amy J NaylorRheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham Research Laboratories, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, B15 2WB, UK.
Jennifer L MarshallRheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham Research Laboratories, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, B15 2WB, UK.
Debbie L HardieRheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham Research Laboratories, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, B15 2WB, UK.
Birgit ZimmermannDepartment of Internal Medicine and Rheumatology, Justus-Liebig-University Giessen, Kerckhoff-Klinik, Bad Nauheim, Germany.
Jason TurnerRheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham Research Laboratories, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, B15 2WB, UK.
Guillaume DesantiRheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham Research Laboratories, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, B15 2WB, UK.
Holly AdamsRheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham Research Laboratories, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, B15 2WB, UK.
Adrian I YemmRheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham Research Laboratories, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, B15 2WB, UK.
Ulf Müller-LadnerDepartment of Internal Medicine and Rheumatology, Justus-Liebig-University Giessen, Kerckhoff-Klinik, Bad Nauheim, Germany.
Jean-Michel DayerFaculty of Medicine, Centre Médical Universitaire, Geneva, Switzerland.
Elena NeumannDepartment of Internal Medicine and Rheumatology, Justus-Liebig-University Giessen, Kerckhoff-Klinik, Bad Nauheim, Germany.
Andrew FilerRheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham Research Laboratories, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, B15 2WB, UK.
Christopher D BuckleyRheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham Research Laboratories, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, B15 2WB, UK. c.d.buckley@bham.ac.uk.
University of Birmingham · GBQueen Elizabeth Hospital Birmingham · GBKerckhoff Klinik · DESandwell & West Birmingham Hospitals NHS Trust · GB

Funding

Arthritis Research UK 18547Arthritis Research UK 19791Arthritis Research UK 20298Versus Arthritis 18547Wellcome Trust WT104551MA
6 · The paper itself

Abstract

backgroundWe investigated two distinct synovial fibroblast populations that were located preferentially in the lining or sub-lining layers and defined by their expression of either podoplanin (PDPN) or CD248, and explored their ability to undergo self-assembly and transmigration in vivo.

methodsSynovial fibroblasts (SF) were cultured in vitro and phenotypic changes following stimulation with interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and transforming growth factor (TGF)-β1 were examined. To examine the phenotype of SF in vivo, a severe combined immunodeficiency (SCID) human-mouse model of cartilage destruction was utilised.

resultsSF in the lining layer in rheumatoid arthritis (RA) expressed high levels of PDPN compared to the normal synovium, whereas CD248 expression was restricted to sub-lining layer cells. TNF-α or IL1 stimulation in vitro resulted in an increased expression of PDPN. In contrast, stimulation with TGF-β1 induced CD248 expression. In the SCID human-mouse model, rheumatoid SF recapitulated the expression of PDPN and CD248. Fibroblasts adjacent to cartilage expressed PDPN, and attached to, invaded, and degraded cartilage. PDPN

conclusionsWe have identified two distinct SF populations identified by expression of either PDPN or CD248 which are located within different anatomical compartments of the inflamed synovial membrane. These markers discriminate between SF subsets with distinct biological properties. As PDPN-expressing cells are associated with early fibroblast migration and cartilage erosion in vivo, we propose that PDPN-expressing cells may be an attractive therapeutic target in RA.

Indexed as

AgedAnimalsAntigens, CDAntigens, NeoplasmArthritis, RheumatoidCartilage, ArticularCell DifferentiationCytokinesFemaleFibroblastsFlow CytometryHeterograftsHumansMaleMembrane GlycoproteinsMiceAntigens, CDAntigens, NeoplasmCD248 protein, humanCytokinesMembrane GlycoproteinsPDPN protein, humanPodoplanin

Identifiers

PMID27863512
PMCPMC5116193
OpenAlexW2556841957

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.