Evidence map›Paper›PMID 34244572›Full record

ArticleScientific reports2021

MicroRNA-378a-3p is overexpressed in psoriasis and modulates cell cycle arrest in keratinocytes via targeting BMP2 gene.

Wipasiri Soonthornchai, Pattarin Tangtanatakul, Kornvalee Meesilpavikkai, Virgil Dalm, Patipark Kueanjinda, Jongkonnee Wongpiyabovorn

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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

6 authors at 2 institutions in 2 countries.

Wipasiri SoonthornchaiDivision of Immunology, Department of Microbiology, Faculty of Medicine, Center of Excellence in Immunology and Immune-Mediated Diseases, Chulalongkorn University, Rama 4 Road, Bangkok, 10330, Thailand.
Pattarin TangtanatakulDivision of Immunology, Department of Microbiology, Faculty of Medicine, Center of Excellence in Immunology and Immune-Mediated Diseases, Chulalongkorn University, Rama 4 Road, Bangkok, 10330, Thailand.
Kornvalee MeesilpavikkaiDivision of Mycology, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
Virgil DalmDivision of Clinical Immunology, Department of Internal Medicine, Erasmus University Medical Center, Rotterdam, The Netherlands.
Patipark KueanjindaDivision of Immunology, Department of Microbiology, Faculty of Medicine, Center of Excellence in Immunology and Immune-Mediated Diseases, Chulalongkorn University, Rama 4 Road, Bangkok, 10330, Thailand.
Jongkonnee WongpiyabovornDivision of Immunology, Department of Microbiology, Faculty of Medicine, Center of Excellence in Immunology and Immune-Mediated Diseases, Chulalongkorn University, Rama 4 Road, Bangkok, 10330, Thailand. jongkonnee.w@chula.ac.th.
Chulalongkorn University · THErasmus MC · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a chronic autoimmune skin disease driven by dysregulations at the cellular, genomic and genetic levels. MicroRNAs are key mediators of gene expression regulation. However, how microRNAs control the pathogenesis of psoriasis is still unclear. Here, we reported a significant up-regulation of miR-378a-3p (miR-378a) in skin biopsies from active psoriatic lesions while it was down-regulated after treatment with methotrexate or narrow-band ultraviolet B phototherapy. Using the keratinocyte in vitro model, we showed that miR-378a disturbed the cell cycle progression, causing cell cycle arrest at G1 phase. Transcriptomic analysis of keratinocytes with miR-378a overexpression and depletion revealed several important biological mechanisms related to inflammation and tight junction. Target mRNA transcript assessed by luciferase assay identified bone morphogenetic protein 2 as a novel target gene of miR-378a. These findings offer a mechanistic model where miR-378a contributes to the pathogenesis of psoriasis.

Indexed as

Bone Morphogenetic Protein 2Cell Cycle CheckpointsGene Expression RegulationHumansKeratinocytesMicroRNAsPsoriasisTranscriptomeUp-RegulationBMP2 protein, humanBone Morphogenetic Protein 2MicroRNAsMIRN378 microRNA, human

Identifiers

PMID34244572
PMCPMC8270917
OpenAlexW3181886062

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.