Evidence map›Paper›PMID 28859619›Full record

ArticleBMC musculoskeletal disorders2017

Analysis of DNA methylation in chondrocytes in rats with knee osteoarthritis.

Xinxin Wang, Dezhi Tang, Peng Shen, Hao Xu, Hongfu Qiu, Tao Wu, Xiang Gao

Open access · goldAbstract read
In one paragraph

Article in BMC musculoskeletal disorders, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

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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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Epigenetics as a Therapeutic Target in Osteoarthritis.Pharmaceuticals (Basel, Switzerland) · 2023
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Effects of Qi-Fang-Xi-Bi-Granules on Cartilage Morphology and C/ebpEvidence-based complementary and alternative medicine : eCAM · 2018
    Article
  10. 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

7 authors at 3 institutions in 1 country.

Xinxin WangDepartment of Surgery, Huadong Hospital Affiliated to Fudan University, Shanghai, 200040, China.
Dezhi TangSpine Research Institute, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China. dztang702@126.com.
Peng ShenDepartment of Surgery, Huadong Hospital Affiliated to Fudan University, Shanghai, 200040, China.
Hao XuSpine Research Institute, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China.
Hongfu QiuDepartment of Surgery, Huadong Hospital Affiliated to Fudan University, Shanghai, 200040, China.
Tao WuDepartment of Surgery, Huadong Hospital Affiliated to Fudan University, Shanghai, 200040, China.
Xiang GaoDepartment of Surgery, Huadong Hospital Affiliated to Fudan University, Shanghai, 200040, China. gaoxiang19710312@sina.com.
Fudan University · CNShanghai University of Traditional Chinese Medicine · CNHuadong Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKnee osteoarthritis (KOA) is a degenerative knee disease commonly found in the ageing population. DNA methylation works with histone acetylation to participate in aging. Alterations of DNA methylation may involve the joint chondrocyte degeneration in KOA. The aim of this study is to detect DNA methylation changes in chondrocytes of rats with KOA.

methodsThe rat KOA model was established with the Hulth method (n = 10), while rats receiving sham operation served as the control (n = 10). At 16 weeks after modeling, the knee joint tissue was collected from half of the rats in each group for Micro-CT scanning, Haematoxylin& Eosin (HE) staining, ABH/OG staining, immunohistochemistry for Bax, Bcl-2 and Fas, and TUNNEL staining. Meanwhile, the articular cartilage was collected from the other half to detect promoter methylation in target genes with the MethylTarget approach.

resultsMicro-CT scanning, HE staining, ABH/OG staining, immunohistochemistry, and TUNNEL staining all showed more severe cartilage injury in the KOA group than in the control group, indicating successful establishment of KOA model. The methylation rate in the KOA group was significantly decreased for C/ebpα-2 (within a CpG island -452 bp to the initiation codon on chromosome 1 91,363,511), Cdk2 (within a CpG island -55 bp to the initiation codon on chromosome 7 3,132,362), Bak1 (within a CpG island 6452 bp to the initiation codon on chromosome 20 5,622,277), and Fas (within a CpG island on the entire chromosome 1 gene), compared with the sham group (P = 0.005, 0.008, 0.022 and 0.027, respectively).

conclusionThe chondrocyte apoptosis and significantly reduced methylation levels of C/ebpα-2, Cdk2, Bak1, and Fas may participate in the pathogenesis of KOA. However, the exact mechanisms remain to be determined.

Indexed as

AnimalsChondrocytesDNA MethylationMaleOsteoarthritis, KneePolymerase Chain ReactionRatsRats, Sprague-DawleyX-Ray MicrotomographyBakCdk2C/ebpαFasKnee osteoarthritisMethylation

Identifiers

PMID28859619
PMCPMC5579940
OpenAlexW2752044135

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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.