Evidence map›Paper›PMID 32134473›Full record

ArticleBioscience reports2020

Down-regulation of protease-activated receptor 2 ameliorated osteoarthritis in rats through regulation of MAPK/NF-κB signaling pathway in vivo and in vitro.

Shichang Yan, Huimin Ding, Junyang Peng, Xinqiang Wang, Chenglong Pang, Juncheng Wei, Jianjun Wei, Hui Chen

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. 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
2.0field-weighted citation impact, top 12% 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, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. PAR2: The Cornerstone of Pancreatic Diseases.Physiological research · 2022
    Review
  9. Article
  10. MiR-19b-3p Attenuates Chondrocytes Injury by Inhibiting MAPK/NF-Κb Axis via Targeting SOCS1.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  11. Article
  12. Article
  13. Protease Activated Receptors and Arthritis.International journal of molecular sciences · 2021
    Review
  14. Review
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 1 institution in 1 country.

Shichang YanDepartment of Orthopaedic, BenQ Medical Center, The Affilicated BenQ Hospital of Nanjing Medical University, 210019, Nanjing, Jiangsu Province, China.
Huimin DingDepartment of Orthopaedic, BenQ Medical Center, The Affilicated BenQ Hospital of Nanjing Medical University, 210019, Nanjing, Jiangsu Province, China.
Junyang PengDepartment of Orthopaedic, BenQ Medical Center, The Affilicated BenQ Hospital of Nanjing Medical University, 210019, Nanjing, Jiangsu Province, China.
Xinqiang WangDepartment of Orthopaedic, BenQ Medical Center, The Affilicated BenQ Hospital of Nanjing Medical University, 210019, Nanjing, Jiangsu Province, China.
Chenglong PangDepartment of Orthopaedic, BenQ Medical Center, The Affilicated BenQ Hospital of Nanjing Medical University, 210019, Nanjing, Jiangsu Province, China.
Juncheng WeiDepartment of Orthopaedic, BenQ Medical Center, The Affilicated BenQ Hospital of Nanjing Medical University, 210019, Nanjing, Jiangsu Province, China.
Jianjun WeiDepartment of Orthopaedic, BenQ Medical Center, The Affilicated BenQ Hospital of Nanjing Medical University, 210019, Nanjing, Jiangsu Province, China.
Hui ChenDepartment of Orthopaedic, BenQ Medical Center, The Affilicated BenQ Hospital of Nanjing Medical University, 210019, Nanjing, Jiangsu Province, China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, protease-activated receptor 2 (PAR2) has been proved to be involved in the inflammatory response including osteoarthritis (OA). In the present study, we found that PAR2 antagonist could remarkably improve the pathological condition of OA rats in vivo. In addition, we also found that PAR2 antagonist could suppress the production of inflammatory factors (TNF-α and Cox-2), decrease the levels of MMP-1 and MMP-13, and restrain the levels of P62 proteins and aggravate the expression of LC3-II both in vivo and in vitro. Besides, in vitro, PAR2 antagonist could increase the proliferation and colony formation of chondrocytes induced with IL-1β. Moreover, PAR2 antagonist could decrease the expression of expressions of p-p38, p-IκBα and p-NF-κB in vitro. However, PAR2 agonist exhibited the opposite effects. Furthermore, SB203580, a p38 MAPK inhibitor, could remarkably promote the proliferation of chondrocytes induced with IL-1β, could alleviate the production of TNF-α and Cox-2, could down-regulate the protein expressions of MMP-1 and MMP-13, and could decrease the expression of P62 and increase the expressions of LC3-II of chondrocytes induced with IL-1β. Importantly, SB203580 could reverse the effects of PAR2 agonist on the functions of chondrocytes induced with IL-1β. Taken together, the present data suggest that down-regulation of PAR2 can ameliorate OA through inducing autophagy via regulation of MAPK/NF-κB signaling pathway in vivo and in vitro, and PAR2 can be considered as a potential candidate to treat OA.

Indexed as

AnimalsChinaChondrocytesCyclooxygenase 2FemaleMaleMAP Kinase Signaling SystemMatrix Metalloproteinase 1Matrix Metalloproteinase 13NF-kappa BOsteoarthritisp38 Mitogen-Activated Protein KinasesRatsRats, Sprague-DawleyReceptor, PAR-2Signal TransductionCyclooxygenase 2Matrix Metalloproteinase 1Matrix Metalloproteinase 13NF-kappa Bp38 Mitogen-Activated Protein KinasesReceptor, PAR-2Tumor Necrosis Factor-alphaAutophagyMAPK/NF-kB signaling pathwayOsteoarthritisProtease-activated receptor 2

Identifiers

PMID32134473
PMCPMC7098131
OpenAlexW3009844301

What OpenQuestion 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 OpenQuestion graph.