Evidence map›Paper›PMID 36474471›Full record

ArticleOsteoarthritis and cartilage open2022

Rheumatoid arthritis chondrocytes produce increased levels of pro-inflammatory proteins.

Karin Önnheim, Shan Huang, Alexander Strid Holmertz, Sofia Andersson, Erik Lönnblom, Charlotte Jonsson, Rikard Holmdahl, Inger Gjertsson

Open access · goldAbstract read
In one paragraph

Article in Osteoarthritis and cartilage open, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

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  11. Emerging Landscape ofACS pharmacology & translational science · 2024
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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

8 authors at 2 institutions in 1 country.

Karin ÖnnheimDep of Rheumatology and Inflammation Research, Institute of Medicine, Gothenburg University, Sweden.
Shan HuangDep of Rheumatology and Inflammation Research, Institute of Medicine, Gothenburg University, Sweden.
Alexander Strid HolmertzDep of Rheumatology and Inflammation Research, Institute of Medicine, Gothenburg University, Sweden.
Sofia AnderssonDep of Rheumatology and Inflammation Research, Institute of Medicine, Gothenburg University, Sweden.
Erik LönnblomMedical Inflammation Research, Dept of Medical Biochemistry and Biophysics, the Karolinska Institute, Stockholm, Sweden.
Charlotte JonssonDep of Rheumatology and Inflammation Research, Institute of Medicine, Gothenburg University, Sweden.
Rikard HolmdahlMedical Inflammation Research, Dept of Medical Biochemistry and Biophysics, the Karolinska Institute, Stockholm, Sweden.
Inger GjertssonDep of Rheumatology and Inflammation Research, Institute of Medicine, Gothenburg University, Sweden.
University of Gothenburg · SEKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To investigate whether articular chondrocytes from rheumatoid arthritis (RA) patients have acquired a proinflammatory phenotype. Method: Articular cartilage explants from RA patients and healthy controls (HC) were cultured with or without interleukin (IL)-1β for two weeks. Protein levels of cytokines and metalloproteinases (MMPs) in the supernatant were measured by LUMINEX, mRNA with qPCR and nitrogen oxide (NO) levels with Griess assay. Results: Within 24 ​h after culture, cartilage explants from RA spontaneously produced MMP-1 and MMP-13, and matrix components (aggrecan and collagen type IV) were released. In addition, the RA explants released higher levels of tumor necrosis factor, interferon-γ, IL-33, IL-18, vascular endothelial growth factor-A, IL-6 but not IL-8, and granulocyte-macrophage colony-stimulating factor (GM-CSF) as compared with HC. During two weeks of incubation the higher levels did not diminish. IL-1β stimulation further increased the levels of IL-6, IL-8 and GM-CSF, mainly in RA explants, and induced increased levels of NO in the supernatant from both HC and RA explants, as a result of chondrocyte activation. Conclusions: RA chondrocytes are activated with a proinflammatory profile involving the production of cytokines as well as MMP-1 and MMP-13, that can lead to release of matrix molecules after activation, which suggests that the chondrocytes have a proinflammatory phenotype and thereby an active role in the pathogenesis.

Indexed as

ChondrocyteCytokineRheumatoid arthritis

Identifiers

PMID36474471
PMCPMC9718183
OpenAlexW4206158561

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.