Evidence map›Paper›PMID 31239367›Full record

ArticleBioscience reports2019

Down-regulation of microRNA-142-3p inhibits the aggressive phenotypes of rheumatoid arthritis fibroblast-like synoviocytes through inhibiting nuclear factor-κB signaling.

Jianhong Qiang, Tingting Lv, Zhenbiao Wu, Xichao Yang

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

  1. Observational
  2. Review
  3. Article
  4. Low expression of miR-142-3p promotes intervertebral disk degeneration.Journal of orthopaedic surgery and research · 2021
    Article
  5. Review
  6. Article
  7. Roles of MicroRNAs in Bone Destruction of Rheumatoid Arthritis.Frontiers in cell and developmental biology · 2020
    Review
  8. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Jianhong QiangDepartment of Traditional Chinese Medicine, Yan'An People's Hospital, No. 57, Qilipu Street, Baota District, Yan'an City 716000, Shaanxi Province, China.
Tingting LvDepartment of Rheumatology and Immunology, The Second Affiliated Hospital of The Fourth Military Medical University, No. 569, Xinsi Road, Xi'an City 710038, Shaanxi Province, China.
Zhenbiao WuDepartment of Clinical Immunology, The First Affiliated Hospital of The Fourth Military Medical University, No. 1, Changle East Road, Xi'an City 710032, Shaanxi Province, China.
Xichao YangDepartment of Clinical Immunology, The First Affiliated Hospital of The Fourth Military Medical University, No. 1, Changle East Road, Xi'an City 710032, Shaanxi Province, China yangxichao258@163.com.ORCID 0000-0001-9187-8457
Air Force Medical University · CNYan'an University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate the regulatory roles of miR-142-3p on the aggressive phenotypes of rheumatoid arthritis (RA) human fibroblast-like synoviocytes (RA-HFLSs), and reveal the potential mechanisms relating with nuclear factor-κB (NF-κB) signaling. miR-142-3p expression was detected in RA synovial tissues and RA-HFLSs by quantitative real-time PCR (qRT-PCR) and Northern blot analysis. RA-HFLSs were transfected with miR-142-3p inhibitor and/or treated with 10 µg/l tumor necrosis factor α (TNF-α). The viability, colony formation, apoptosis, migration, invasion, and the levels of interleukin (IL)-6, and matrix metalloproteinase 3 (MMP-3) were detected. The mRNA expressions of B-cell lymphoma-2 (Bcl-2), Bax, Bad, IL-6, and MMP-3 were detected by qRT-PCR. Moreover, the expression of Bcl-2, IL-1 receptor-associated kinase 1 (IRAK1), Toll-like receptor 4 (TLR4), NF-κB p65, and phosphorylated NF-κB p65 (p-NF-κB p65) were detected by Western blot. The interaction between IRAK1 and miR-142-3p was identified by dual luciferase reporter gene assay. MiR-142-3p was up-regulated in RA synovial tissues and RA-HFLSs. TNF-α activated the aggressive phenotypes of RA-HFLSs, including enhanced proliferation, migration, invasion, and inflammation, and inhibited apoptosis. miR-142-3p inhibitor significantly decreased the cell viability, the number of cell clones, the migration rate, the number of invasive cells, the contents and expression of IL-6 and MMP-3, and increased the apoptosis rate and the expressions of Bax and Bad, and decreased Bcl-2 expression of TNF-α-treated RA-HFLSs. MiR-142-3p inhibitor significantly reversed TNF-α-induced up-regulation of IRAK1, TLR4, and p-NF-κB p65 in TNF-α-treated RA-HFLSs. Besides, IRAK1 was a target of miR-142-3p. The down-regulation of miR-142-3p inhibited the aggressive phenotypes of RA-HFLSs through inhibiting NF-κB signaling.

Indexed as

Arthritis, RheumatoidCell ProliferationFemaleFibroblastsGene Expression RegulationHumansInflammationInterleukin-1 Receptor-Associated KinasesMaleMatrix Metalloproteinase 3MicroRNAsMiddle AgedNF-kappa BSignal TransductionSynovial MembraneSynoviocytesInterleukin-1 Receptor-Associated KinasesIRAK1 protein, humanMatrix Metalloproteinase 3MicroRNAsMIRN142 microRNA, humanMMP3 protein, humanNF-kappa BTumor Necrosis Factor-alphaInflammationMicroRNA-142-3pNuclear factor-kappa BProliferationTumor necrosis factor α

Identifiers

PMID31239367
PMCPMC6614573
OpenAlexW2954968972

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.