Evidence map›Paper›PMID 37151687›Full record

ArticleHeliyon2023

Exosomes derived from synovial fibroblasts from patients with rheumatoid arthritis promote macrophage migration that can be suppressed by miR-124-3p.

Yuji Nakamachi, Kenichi Uto, Shinya Hayashi, Takaichi Okano, Akio Morinobu, Ryosuke Kuroda, Seiji Kawano, Jun Saegusa

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
4.8field-weighted citation impact, top 5% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.

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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 2 institutions in 1 country.

Yuji NakamachiDepartment of Clinical Laboratory, Kobe University Hospital, 7-5-2, Kusunoki cho, Chuo Ku, Kobe 650-0017, Japan.
Kenichi UtoDepartment of Clinical Laboratory, Kobe University Hospital, 7-5-2, Kusunoki cho, Chuo Ku, Kobe 650-0017, Japan.
Shinya HayashiDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki cho, Chuo Ku, Kobe 650-0017, Japan.
Takaichi OkanoDepartment of Clinical Laboratory, Kobe University Hospital, 7-5-2, Kusunoki cho, Chuo Ku, Kobe 650-0017, Japan.
Akio MorinobuDepartment of Rheumatology and Clinical Immunology, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki cho, Chuo Ku, Kobe 650-0017, Japan.
Ryosuke KurodaDepartment of Orthopaedic Surgery, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki cho, Chuo Ku, Kobe 650-0017, Japan.
Seiji KawanoDepartment of Medical Education, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki cho, Chuo Ku, Kobe 650-0017, Japan.
Jun SaegusaDepartment of Rheumatology and Clinical Immunology, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki cho, Chuo Ku, Kobe 650-0017, Japan.
Kobe University · JPKobe University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: Exosomes are potent vehicles for intercellular communication. Rheumatoid arthritis (RA) is a chronic systemic disease of unknown etiology. Local administration of miR-124 precursor to rats with adjuvant-induced arthritis suppresses systemic arthritis and bone destruction. Thus, exosomes may be involved in this disease. We aimed to determine the role of exosomes in the pathology of RA. Methods: Fibroblast-like synoviocytes (FLS) were collected from patients with RA and osteoarthritis (OA). miR-124-3p mimic was transfected into the RA FLS (RA miR-124 FLS). Exosomes were collected from the culture medium by ultracentrifugation. Macrophages were produced from THP-1 cells. MicroRNAs in the exosomes were analyzed using real-time PCR. Proteomics analysis was performed using nanoscale liquid chromatography-tandem mass spectrometry. Macrophage migration was evaluated using a Transwell migration assay. SiRNA was used to knockdown proteins of interest. Results: MicroRNAs in the RA FLS, RA miR-124 FLS, and OA FLS exosomes were similar. Proteomics analysis revealed that pentraxin 3 (PTX3) levels were higher in RA FLS exosomes than in RA miR-124 FLS and OA FLS exosomes, and proteasome 20S subunit beta 5 (PSMB5) levels were lower in RA FLS exosomes than in RA miR-124 FLS and OA FLS exosomes. The RA FLS exosomes promoted and the RA miR-124 FLS exosomes suppressed macrophage migration. PTX3-silenced RA FLS exosomes suppressed and PSMB5-silenced OA FLS exosomes promoted macrophage migration. Conclusions: RA FLS exosomes promote macrophage migration via PTX3 and PSMB5, and miR-124-3p suppresses this migration.

Indexed as

ExosomeFibroblast-like synoviocytesMacrophageMigrationmiR-124-3pRheumatoid arthritis

Identifiers

PMID37151687
PMCPMC10161379
OpenAlexW4361290653

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.