Evidence map›Paper›PMID 24374632›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Identification of key regulators for the migration and invasion of rheumatoid synoviocytes through a systems approach.

Sungyong You, Seung-Ah Yoo, Susanna Choi, Ji-Young Kim, Su-Jung Park, Jong Dae Ji, Tae-Hwan Kim, Ki-Jo Kim, Chul-Soo Cho, Daehee Hwang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

  1. Meta-Analysis ofFrontiers in immunology · 2019
    Pooled it
  2. Trial
  3. Review
  4. Galectin-9 inhibition of the MIF-CD74/CD44 pathway suppresses chronic arthritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
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  13. Review
  14. Article
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  16. Article
  17. Alcohol extracts fromMolecular medicine reports · 2023
    Article
  18. Article
  19. Article
  20. The use of animal models in rheumatoid arthritis research.Journal of Yeungnam medical science · 2023
    Article

8 more citing papers are in PubMed but not listed here.

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

11 authors at 5 institutions in 1 country.

Sungyong YouSchool of Interdisciplinary Bioscience and Bioengineering, Pohang University of Science and Technology, Pohang 790-784, Korea.
Seung-Ah Yoo
Susanna Choi
Ji-Young Kim
Su-Jung Park
Jong Dae Ji
Tae-Hwan Kim
Ki-Jo Kim
Chul-Soo Cho
Daehee Hwang
Wan-Uk Kim
Catholic University of Korea · KRHanyang University Seoul Hospital · KRInstitute for Basic Science · KRKorea University · KRPohang University of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid synoviocytes, which consist of fibroblast-like synoviocytes (FLSs) and synovial macrophages (SMs), are crucial for the progression of rheumatoid arthritis (RA). Particularly, FLSs of RA patients (RA-FLSs) exhibit invasive characteristics reminiscent of cancer cells, destroying cartilage and bone. RA-FLSs and SMs originate differently from mesenchymal and myeloid cells, respectively, but share many pathologic functions. However, the molecular signatures and biological networks representing the distinct and shared features of the two cell types are unknown. We performed global transcriptome profiling of FLSs and SMs obtained from RA and osteoarthritis patients. By comparing the transcriptomes, we identified distinct molecular signatures and cellular processes defining invasiveness of RA-FLSs and proinflammatory properties of RA-SMs, respectively. Interestingly, under the interleukin-1β (IL-1β)-stimulated condition, the RA-FLSs newly acquired proinflammatory signature dominant in RA-SMs without losing invasive properties. We next reconstructed a network model that delineates the shared, RA-FLS-dominant (invasive), and RA-SM-dominant (inflammatory) processes. From the network model, we selected 13 genes, including periostin, osteoblast-specific factor (POSTN) and twist basic helix-loop-helix transcription factor 1 (TWIST1), as key regulator candidates responsible for FLS invasiveness. Of note, POSTN and TWIST1 expressions were elevated in independent RA-FLSs and further instigated by IL-1β. Functional assays demonstrated the requirement of POSTN and TWIST1 for migration and invasion of RA-FLSs stimulated with IL-1β. Together, our systems approach to rheumatoid synovitis provides a basis for identifying key regulators responsible for pathological features of RA-FLSs and -SMs, demonstrating how a certain type of cells acquires functional redundancy under chronic inflammatory conditions.

Indexed as

Gene Expression RegulationArthritis, RheumatoidCell Adhesion MoleculesCell MovementCluster AnalysisFibroblastsGene Expression ProfilingHumansInflammationInterleukin-1betaIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsMacrophagesModels, BiologicalNuclear ProteinsOsteoarthritisCell Adhesion MoleculesInterleukin-1betaIntracellular Signaling Peptides and ProteinsLIM Domain ProteinsNuclear ProteinsPOSTN protein, humanTGFB1I1 protein, humanTWIST1 protein, humanTwist-Related Protein 1

Identifiers

PMID24374632
PMCPMC3890851
OpenAlexW1981094412

What OpenQuestion holds

Textmetadata
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.