Evidence map›Paper›PMID 26976200›Full record

ArticleScientific reports2016

NOD-like receptor signaling and inflammasome-related pathways are highlighted in psoriatic epidermis.

Mari H Tervaniemi, Shintaro Katayama, Tiina Skoog, H Annika Siitonen, Jyrki Vuola, Kristo Nuutila, Raija Sormunen, Anna Johnsson, Sten Linnarsson, Sari Suomela and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 92 citations in OpenAlex.

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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

13 authors at 6 institutions in 2 countries.

Mari H TervaniemiFolkhälsan Institute of Genetics, Helsinki, Finland.
Shintaro KatayamaDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Tiina SkoogDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
H Annika SiitonenFolkhälsan Institute of Genetics, Helsinki, Finland.
Jyrki VuolaHelsinki Burn Center, Department of Plastic Surgery, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Kristo NuutilaDepartment of Pharmacology, Medicum, University of Helsinki, Helsinki, Finland.
Raija SormunenBiocenter Oulu, Department of Pathology, University of Oulu, Oulu, Finland.
Anna JohnssonDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Sten LinnarssonDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Sari SuomelaDepartment of Dermatology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Esko KankuriDepartment of Pharmacology, Medicum, University of Helsinki, Helsinki, Finland.
Juha KereFolkhälsan Institute of Genetics, Helsinki, Finland.
Outi ElomaaFolkhälsan Institute of Genetics, Helsinki, Finland.
University of Helsinki · FIKarolinska Institutet · SEScience for Life Laboratory · SEFolkhälsans Forskningscentrum · FIHelsinki University Hospital · FIUniversity of Oulu · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriatic skin differs distinctly from normal skin by its thickened epidermis. Most gene expression comparisons utilize full-thickness biopsies, with substantial amount of dermis. We assayed the transcriptomes of normal, lesional, and non-lesional psoriatic epidermis, sampled as split-thickness skin grafts, with 5'-end RNA sequencing. We found that psoriatic epidermis contains more mRNA per total RNA than controls, and took this into account in the bioinformatic analysis. The approach highlighted innate immunity-related pathways in psoriasis, including NOD-like receptor (NLR) signaling and inflammasome activation. We demonstrated that the NLR signaling genes NOD2, PYCARD, CARD6, and IFI16 are upregulated in psoriatic epidermis, and strengthened these findings by protein expression. Interestingly, PYCARD, the key component of the inflammasome, showed an altered expression pattern in the lesional epidermis. The profiling of non-lesional skin highlighted PSORS4 and mitochondrially encoded transcripts, suggesting that their gene expression is altered already before the development of lesions. Our data suggest that all components needed for the active inflammasome are present in the keratinocytes of psoriatic skin. The characterization of inflammasome pathways provides further opportunities for therapy. Complementing previous transcriptome studies, our approach gives deeper insight into the gene regulation in psoriatic epidermis.

Indexed as

AgedCARD Signaling Adaptor ProteinsCytoskeletal ProteinsEpidermisFemaleGene Expression ProfilingHumansImmunohistochemistryInflammasomesKeratinocytesMaleMicroscopy, ConfocalMicroscopy, ImmunoelectronMiddle AgedNLR ProteinsNod2 Signaling Adaptor ProteinCARD6 protein, humanCARD Signaling Adaptor ProteinsCytoskeletal ProteinsIFI16 protein, humanInflammasomesNLR ProteinsNOD2 protein, humanNod2 Signaling Adaptor ProteinNuclear ProteinsPhosphoproteinsPYCARD protein, humanRNA, Messenger

Identifiers

PMID26976200
PMCPMC4792137
OpenAlexW2298576674

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.