Evidence map›Paper›PMID 24933320›Full record

ArticleThe Journal of investigative dermatology2014

Abnormally differentiating keratinocytes in the epidermis of systemic sclerosis patients show enhanced secretion of CCN2 and S100A9.

Joanna Nikitorowicz-Buniak, Xu Shiwen, Christopher P Denton, David Abraham, Richard Stratton

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  16. Article
  17. Current Concepts on the Pathogenesis of Systemic Sclerosis.Clinical reviews in allergy & immunology · 2023
    Review
  18. Article
  19. Review
  20. Contribution of keratinocytes to dermal fibrosis.Current opinion in rheumatology · 2022
    Review
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

5 authors at 1 institution in 1 country.

Joanna Nikitorowicz-BuniakCentre for Rheumatology and Connective Tissue Diseases, Research Department of Inflammation, Division of Medicine, UCL-Medical School, London, UK. Electronic address: j.nikitorowicz-buniak@ucl.ac.uk.
Xu ShiwenCentre for Rheumatology and Connective Tissue Diseases, Research Department of Inflammation, Division of Medicine, UCL-Medical School, London, UK.
Christopher P DentonCentre for Rheumatology and Connective Tissue Diseases, Research Department of Inflammation, Division of Medicine, UCL-Medical School, London, UK.
David AbrahamCentre for Rheumatology and Connective Tissue Diseases, Research Department of Inflammation, Division of Medicine, UCL-Medical School, London, UK.
Richard StrattonCentre for Rheumatology and Connective Tissue Diseases, Research Department of Inflammation, Division of Medicine, UCL-Medical School, London, UK.
Centre for Inflammation Research · GB

Funding

Medical Research Council G0801052Versus Arthritis 19427
6 · The paper itself

Abstract

Skin involvement with dermal fibrosis is a hallmark of systemic sclerosis (SSc), and keratinocytes may be critical regulators of fibroblast function through secretion of chemo-attracting agents, as well as through growth factors and cytokines influencing the phenotype and proliferation rate of fibroblasts. Epithelial-fibroblast interactions have an important role in fibrosis in general. We have characterized the SSc epidermis and asked whether SSc-injured epidermal cells release factors capable of promoting fibrosis. Our results show that the SSc epidermis is hypertrophic, and has altered expression of terminal differentiation markers involucrin, loricrin, and filaggrin. Multiplex profiling revealed that SSc epidermal explants release increased levels of CCN2 and S100A9. CCN2 induction was found to spread into the upper papillary dermis, whereas S100A9 was shown to induce fibroblast proliferation and to enhance fibroblast CCN2 expression via Toll-like receptor 4. These data suggest that the SSc epidermis provides an important source of pro-fibrotic CCN2 and proinflammatory S100A9 in SSc skin, and therefore contributes to the fibrosis and inflammation seen in the disease.

Indexed as

Epidermal CellsCalgranulin BCell DifferentiationCell ProliferationConnective Tissue Growth FactorDermisEpidermisFibroblastsFibrosisFilaggrin ProteinsHepatocyte Growth FactorHumansInflammationKeratinocytesScleroderma, SystemicSkinCalgranulin BCCN2 protein, humanConnective Tissue Growth FactorFilaggrin ProteinsFLG protein, humanHepatocyte Growth FactorTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID24933320
OpenAlexW2310239780

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.