Evidence map›Paper›PMID 34199748›Full record

ArticleInternational journal of molecular sciences2021

Dysregulation of Connexin Expression Plays a Pivotal Role in Psoriasis.

Erin M O'Shaughnessy, William Duffy, Laura Garcia-Vega, Keith Hussey, A David Burden, Mozheh Zamiri, Patricia E Martin

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Skin Barrier Dysregulation in Psoriasis.International journal of molecular sciences · 2021
    Review
  7. Purinergic Signaling and Inflammasome Activation in Psoriasis Pathogenesis.International journal of molecular sciences · 2021
    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

7 authors at 4 institutions in 1 country.

Erin M O'ShaughnessyDepartment of Biological and Biomedical Sciences, School of Health and Life Sciences, Glasgow Caledonian University, Glasgow G4 0BA, UK.
William DuffyDepartment of Dermatology, University Hospital Crosshouse, Kilmarnock KA2 0BE, UK.
Laura Garcia-VegaDepartment of Biological and Biomedical Sciences, School of Health and Life Sciences, Glasgow Caledonian University, Glasgow G4 0BA, UK.
Keith HusseyDepartment of Vascular Surgery, Queen Elizabeth University Hospital, Glasgow G51 4TF, UK.
A David BurdenInstitute of Infection Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK.
Mozheh ZamiriDepartment of Dermatology, University Hospital Crosshouse, Kilmarnock KA2 0BE, UK.
Patricia E MartinDepartment of Biological and Biomedical Sciences, School of Health and Life Sciences, Glasgow Caledonian University, Glasgow G4 0BA, UK.ORCID 0000-0003-0890-8059
Glasgow Caledonian University · GBUniversity Hospital Crosshouse · GBQueen Elizabeth University Hospital · GBUniversity of Glasgow · GB

Funding

Psoriasis Association ST3 15
6 · The paper itself

Abstract

backgroundPsoriasis, a chronic inflammatory disease affecting 2-3% of the population, is characterised by epidermal hyperplasia, a sustained pro-inflammatory immune response and is primarily a T-cell driven disease. Previous work determined that Connexin26 is upregulated in psoriatic tissue. This study extends these findings.

methodsBiopsies spanning psoriatic plaque (PP) and non-involved tissue (PN) were compared to normal controls (NN). RNA was isolated and subject to real-time PCR to determine gene expression profiles, including

resultsConnexin26 expression is dramatically enhanced at both transcriptional and translational level in PP and PN tissue compared to NN (>100x). In contrast, CX43 gene expression is not affected, but the protein is post-translationally modified and accumulates in psoriatic tissue. Fibroblasts isolated from psoriatic patients had a higher inflammatory index than normal fibroblasts and drove normal keratinocytes to adopt a "psoriatic phenotype" in a 3D-organotypic model. Exposure of normal fibroblasts to the pro-inflammatory mediator peptidoglycan, isolated from

conclusiondysregulation of the connexin26:43 expression profile in psoriatic tissue contributes to an imbalance of cellular events. Inhibition of connexin signalling reduces pro-inflammatory events and may hold therapeutic benefit.

Indexed as

Gene Expression RegulationAdultAgedBiopsyConnexinsEpidermisFibroblastsGene Expression ProfilingHaCaT CellsHumansInflammation MediatorsKeratinocytesMiddle AgedModels, BiologicalOligopeptidesPeptidoglycanConnexinsgap 27 peptideInflammation MediatorsOligopeptidesPeptidoglycanconnexin26connexin43connexin mimetic peptideepidermisgap junctionhemichannelspsoriasis

Identifiers

PMID34199748
PMCPMC8200029
OpenAlexW3168383725

What Socratic 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 Socratic graph.