Evidence map›Paper›PMID 29706965›Full record

ArticleFrontiers in immunology2018

Transcription Factor SOX5 Promotes the Migration and Invasion of Fibroblast-Like Synoviocytes in Part by Regulating MMP-9 Expression in Collagen-Induced Arthritis.

Yumeng Shi, Qin Wu, Wenhua Xuan, Xiaoke Feng, Fang Wang, Betty P Tsao, Miaojia Zhang, Wenfeng Tan

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

25 citing papers in PubMed, 47 citations in OpenAlex.

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  7. LED irradiation at 630 nm alleviates collagen-induced arthritis in mice by inhibition of NF-κB-mediated MMPs production.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2023
    Article
  8. Article
  9. Article
  10. SOX2 Overlapping Transcript (Iranian journal of biotechnology · 2023
    Article
  11. Article
  12. Article
  13. Article
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  15. The Immunogenetics of Systemic Sclerosis.Advances in experimental medicine and biology · 2022
    Article
  16. Article
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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 4 institutions in 2 countries.

Yumeng ShiDepartment of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Qin WuDepartment of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wenhua XuanDepartment of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Xiaoke FengDepartment of Traditional Chinese Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Fang WangDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Betty P TsaoDivision of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Miaojia ZhangDepartment of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wenfeng TanDepartment of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jiangsu Province Hospital · CNNanjing Medical University · CNMedical University of South Carolina · USNanjing Traditional Chinese Medicine Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: Fibroblast-like synoviocytes (FLS) exhibit a unique aggressive phenotype in rheumatoid arthritis (RA). Increased FLS migration and subsequent invasion of the extracellular matrix are essential to joint destruction in RA. Our previous research reported that transcription factor SOX5 was highly expressed in RA-FLS. Here, the effects of SOX5 in RA-FLS migration and invasion will be investigated. Methods: The migration and invasion of RA-FLS were evaluated using a transwell chamber assay. The expression of several potential SOX5-targeted genes, including matrix metalloproteinases (MMP-1, 2, 3 and 9), chemokines (CCL4, CCL2, CCR5 and CCR2), and pro-inflammatory cytokines (TNF-α and IL-6), were examined in RA-FLS using SOX5 gain- and loss-of-function study. The molecular mechanisms of SOX5-mediated MMP-9 expressions were assayed by luciferase reporter gene and chromatin immunoprecipitation (ChIP) studies. The Results: Knockdown SOX5 decreased lamellipodium formation, migration, and invasion of RA-FLS. The expression of MMP-9 was the only gene tested to be concomitantly affected by silencing or overexpressing SOX5. ChIP assay revealed that SOX5 was bound to the MMP-9 promoter in RA-FLS. The overexpression of SOX5 markedly enhanced the MMP-9 promoter activity, and specific deletion of a putative SOX5-binding site in MMP-9 promoter diminished this promoter-driven transcription in FLS. Locally knocked down SOX5 inhibited MMP-9 expression in the joint tissue and reduced pannus migration and invasion into the cartilage in CIA mice. Conclusion: SOX5 plays a novel role in mediating migration and invasion of FLS in part by regulating MMP-9 expression in RA.

Indexed as

AnimalsAnkle JointArthritis, ExperimentalArthritis, RheumatoidCell MovementCells, CulturedHumansMaleMatrix Metalloproteinase 9Mice, Inbred DBASOXD Transcription FactorsSynoviocytesMatrix Metalloproteinase 9Mmp9 protein, mouseSox5 protein, mouseSOXD Transcription Factorsfibroblast-like synoviocytesmatrix metalloproteinase-9migration and invasionrheumatoid arthritistranscription factor SOX5

Identifiers

PMID29706965
PMCPMC5906798
OpenAlexW2797098066

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.