Evidence map›Paper›PMID 36614150›Full record

ArticleInternational journal of molecular sciences2022

S100A8 and S100A12 Proteins as Biomarkers of High Disease Activity in Patients with Rheumatoid Arthritis That Can Be Regulated by Epigenetic Drugs.

Leszek Roszkowski, Bożena Jaszczyk, Magdalena Plebańczyk, Marzena Ciechomska

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 22 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

4 authors at 1 institution in 1 country.

Leszek RoszkowskiDepartment of Outpatient Clinics, National Institute of Geriatrics, Rheumatology and Rehabilitation (NIGRiR), 02-637 Warsaw, Poland.
Bożena JaszczykDepartment of Outpatient Clinics, National Institute of Geriatrics, Rheumatology and Rehabilitation (NIGRiR), 02-637 Warsaw, Poland.ORCID 0000-0002-2009-0723
Magdalena PlebańczykDepartment of Pathophysiology and Immunology, National Institute of Geriatrics, Rheumatology and Rehabilitation (NIGRiR), 02-637 Warsaw, Poland.
Marzena CiechomskaDepartment of Pathophysiology and Immunology, National Institute of Geriatrics, Rheumatology and Rehabilitation (NIGRiR), 02-637 Warsaw, Poland.ORCID 0000-0002-0961-6130
National Institute of Geriatrics, Rheumatology and Rehabilitation · PL

Funding

National Centre for Nuclear Research 2018/30/E/NZ5/00104
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune chronic inflammatory disease that is still not well understood in terms of its pathogenesis and presents diagnostic and therapeutic challenges. Monocytes are key players in initiating and maintaining inflammation through the production of pro-inflammatory cytokines and S100 proteins in RA. This study aimed to test a specific DNA methylation inhibitor (RG108) and activator (budesonide) in the regulation of pro-inflammatory mediators-especially the S100 proteins. We also searched for new biomarkers of high disease activity in RA patients. RNA sequencing analysis of healthy controls (HCs) and RA monocytes was performed. Genes such as the S100 family, TNF, and IL-8 were validated by qRT-PCR following DNA-methylation-targeted drug treatment in a monocytic THP-1 cell line. The concentrations of the S100A8, S100A11, and S100A12 proteins in the sera and synovial fluids of RA patients were tested and correlated with clinical parameters. We demonstrated that RA monocytes had significantly increased levels of S100A8, S100A9, S100A11, S100A12, MYD88, JAK3, and IQGAP1 and decreased levels of IL10RA and TGIF1 transcripts. In addition, stimulation of THP-1 cells with budesonide statistically reduced the expression of the S100 family, IL-8, and TNF genes. In contrast, THP-1 cells treated with RG108 had increased levels of the S100 family and TNF genes. We also revealed a significant upregulation of S100A8, S100A11, and S100A12 in RA patients, especially in early RA compared to HC sera. In addition, protein levels of S100A8, S100A11, and S100A12 in RA synovial fluids compared to HC sera were significantly increased. Overall, our data suggest that the S100A8 and S100A12 proteins are strongly elevated during ongoing inflammation, so they could be used as a better biomarker of disease activity than CRP. Interestingly, epigenetic drugs can regulate these S100 proteins, suggesting their potential use in targeting RA inflammation.

Indexed as

Arthritis, RheumatoidS100A12 ProteinBiomarkersBudesonideCalgranulin ACalgranulin BEpigenesis, GeneticHomeodomain ProteinsHumansInflammationInterleukin-8PhthalimidesRepressor ProteinsS100 ProteinsTryptophanBiomarkersBudesonideCalgranulin ACalgranulin BHomeodomain ProteinsInterleukin-8PhthalimidesRepressor ProteinsRG108S100A12 ProteinS100A12 protein, humanS100 ProteinsTGIF1 protein, humanTryptophanbiomarkersDNA methylationepigeneticsmonocytesrheumatoid arthritisS100 proteinstranscriptomics

Identifiers

PMID36614150
PMCPMC9820830
OpenAlexW4313471729

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.