Evidence map›Paper›PMID 27433031›Full record

ArticleMediators of inflammation2016

Interleukin-29 Enhances Synovial Inflammation and Cartilage Degradation in Osteoarthritis.

Lingxiao Xu, Qiuyue Peng, Wenhua Xuan, Xiaoke Feng, Xiangqing Kong, Miaojia Zhang, Wenfeng Tan, Meilang Xue, Fang Wang

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Reply.Arthritis & rheumatology (Hoboken, N.J.) · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Insights into IL-29: Emerging role in inflammatory autoimmune diseases.Journal of cellular and molecular medicine · 2019
    Review
  12. Inhibition of MMPs and ADAM/ADAMTS.Biochemical pharmacology · 2019
    Review
  13. Article
  14. Article
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

9 authors at 2 institutions in 2 countries.

Lingxiao XuDepartment of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Qiuyue PengDepartment of Traditional Chinese Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Wenhua XuanDepartment of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Xiaoke FengDepartment of Traditional Chinese Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Xiangqing KongDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.ORCID 0000-0002-5433-5557
Miaojia ZhangDepartment of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Wenfeng TanDepartment of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Meilang XueSutton Arthritis Research Laboratories, University of Sydney at Royal North Shore Hospital, Sydney, NSW, Australia.
Fang WangDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.ORCID 0000-0002-0526-7607
Jiangsu Province Hospital · CNThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have recently shown that IL-29 was an important proinflammatory cytokine in pathogenesis of rheumatoid arthritis (RA). Inflammation also contributes to the pathogenesis of osteoarthritis (OA). The aim of this study was to investigate the effect and mechanism of IL-29 on cytokine production and cartilage degradation in OA. The mRNA levels of IL-29 and its specific receptor IL-28Ra in peripheral blood mononuclear cells (PBMCs) were significantly increased in OA patients when compared to healthy controls (HC). In the serum, IL-29 protein levels were higher in OA patients than those in HC. Immunohistochemistry revealed that both IL-29 and IL-28Ra were dramatically elevated in OA synovium compared to HC; synovial fibroblasts (FLS) and macrophages were the main IL-29-producing cells in OA synovium. Furthermore, recombinant IL-29 augmented the mRNA expression of IL-1β, IL-6, IL-8, and matrix-metalloproteinase-3 (MMP-3) in OA FLS and increased cartilage degradation when ex vivo OA cartilage explant was coincubated with OA FLS. Finally, in OA FLS, IL-29 dominantly activated MAPK and nuclear factor-κB (NF-κB), but not Jak-STAT and AKT signaling pathway as examined by western blot. In conclusion, IL-29 stimulates inflammation and cartilage degradation by OA FLS, indicating that this cytokine is likely involved in the pathogenesis of OA.

Indexed as

AgedCartilageCells, CulturedFemaleFibroblastsFlow CytometryHumansInflammationInterferon LambdaInterferonsInterleukin-1betaInterleukin-6Interleukin-8InterleukinsIn Vitro TechniquesLeukocytes, MononuclearInterferon Lambdainterferon-lambda, humanInterferonsInterleukin-1betainterleukin 28alpha receptorInterleukin-6Interleukin-8InterleukinsMatrix Metalloproteinase 3Receptors, Cytokine

Identifiers

PMID27433031
PMCPMC4940582
OpenAlexW2460325737

What OpenQuestion holds

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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.