Evidence map›Paper›PMID 37060003›Full record

ArticleArthritis research & therapy2023

Activated CD90/Thy-1 fibroblasts co-express the Δ133p53β isoform and are associated with highly inflamed rheumatoid arthritis.

Anna K Wiles, Sunali Mehta, Melanie Millier, Adele G Woolley, Kunyu Li, Kim Parker, Marina Kazantseva, Michelle Wilson, Katie Young, Sarah Bowie and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arthritis research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
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

15 authors at 2 institutions in 1 country.

Anna K WilesDepartment of Pathology, University of Otago, Hercus Building, 58 Hanover Street, Dunedin, New Zealand.
Sunali MehtaDepartment of Pathology, University of Otago, Hercus Building, 58 Hanover Street, Dunedin, New Zealand.
Melanie MillierDepartment of Medicine, University of Otago, Dunedin, New Zealand.
Adele G WoolleyDepartment of Pathology, University of Otago, Hercus Building, 58 Hanover Street, Dunedin, New Zealand.
Kunyu LiDepartment of Pathology, University of Otago, Hercus Building, 58 Hanover Street, Dunedin, New Zealand.
Kim ParkerDepartment of Pathology, University of Otago, Hercus Building, 58 Hanover Street, Dunedin, New Zealand.
Marina KazantsevaDepartment of Pathology, University of Otago, Hercus Building, 58 Hanover Street, Dunedin, New Zealand.
Michelle WilsonDepartment of Pathology, University of Otago, Hercus Building, 58 Hanover Street, Dunedin, New Zealand.
Katie YoungDepartment of Pathology, University of Otago, Hercus Building, 58 Hanover Street, Dunedin, New Zealand.
Sarah BowieDepartment of Pathology, University of Otago, Hercus Building, 58 Hanover Street, Dunedin, New Zealand.
Sankalita RayDepartment of Pathology, University of Otago, Hercus Building, 58 Hanover Street, Dunedin, New Zealand.
Tania L SlatterDepartment of Pathology, University of Otago, Hercus Building, 58 Hanover Street, Dunedin, New Zealand.
Lisa K StampDepartment of Medicine, University of Otago, Christchurch, New Zealand.
Paul A HessianDepartment of Medicine, University of Otago, Dunedin, New Zealand.
Antony W BraithwaiteDepartment of Pathology, University of Otago, Hercus Building, 58 Hanover Street, Dunedin, New Zealand. antony.braithwaite@otago.ac.nz.
University of Otago · NZMaurice Wilkins Centre · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe p53 isoform Δ133p53β is known to be associated with cancers driven by inflammation. Many of the features associated with the development of inflammation in rheumatoid arthritis (RA) parallel those evident in cancer progression. However, the role of this isoform in RA has not yet been explored. The aim of this study was to determine whether Δ133p53β is driving aggressive disease in RA.

methodsUsing RA patient synovia, we carried out RT-qPCR and RNAScope-ISH to determine both protein and mRNA levels of Δ133p53 and p53. We also used IHC to determine the location and type of cells with elevated levels of Δ133p53β. Plasma cytokines were also measured using a BioPlex cytokine panel and data analysed by the Milliplex Analyst software.

resultsElevated levels of pro-inflammatory plasma cytokines were associated with synovia from RA patients displaying extensive tissue inflammation, increased immune cell infiltration and the highest levels of Δ133TP53 and TP53β mRNA. Located in perivascular regions of synovial sub-lining and surrounding ectopic lymphoid structures (ELS) were a subset of cells with high levels of CD90, a marker of 'activated fibroblasts' together with elevated levels of Δ133p53β.

conclusionsInduction of Δ133p53β in CD90

Indexed as

Arthritis, RheumatoidTumor Suppressor Protein p53Cells, CulturedCytokinesFibroblastsHumansInflammationProtein IsoformsRNA, MessengerSynovial MembraneThy-1 AntigensCytokinesProtein IsoformsRNA, MessengerThy-1 AntigensTumor Suppressor Protein p53CD90FibroblastsInflammationp53 isoformsRheumatoid arthritisSynoviocytes

Identifiers

PMID37060003
PMCPMC10105423
OpenAlexW4365810838

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.