Evidence map›Paper›PMID 34670484›Full record

ArticleMolecular medicine (Cambridge, Mass.)2021

Deregulation of circ_003912 contributes to pathogenesis of erosive oral lichen planus by via sponging microRNA-123, -647 and -31 and upregulating FOXP3.

Zhen Huang, Fen Liu, Wenjuan Wang, Shaobo Ouyang, Ting Sang, Zikun Huang, Lan Liao, Jun Wu

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
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  13. The Functional Mechanism of MicroRNA in Oral Lichen Planus.Journal of inflammation research · 2022
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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 1 institution in 1 country.

Zhen HuangJiangxi Provincial Key Laboratory of Oral Biomedicine, Department of Orthodontics, the Affiliated Stomatological Hospital of Nanchang University, Nanchang, 330006, China.
Fen LiuJiangxi Provincial Key Laboratory of Oral Biomedicine, Department of Orthodontics, the Affiliated Stomatological Hospital of Nanchang University, Nanchang, 330006, China.
Wenjuan WangJiangxi Provincial Key Laboratory of Oral Biomedicine, Department of Orthodontics, the Affiliated Stomatological Hospital of Nanchang University, Nanchang, 330006, China.
Shaobo OuyangJiangxi Provincial Key Laboratory of Oral Biomedicine, Department of Oral Prosthodontics, the Affiliated Stomatological Hospital of Nanchang University, Nanchang, 330006, China.
Ting SangJiangxi Provincial Key Laboratory of Oral Biomedicine, Department of Orthodontics, the Affiliated Stomatological Hospital of Nanchang University, Nanchang, 330006, China.
Zikun HuangClinical Laboratory Center, the First Affiliated Hospital of Nanchang University, No.49 Fuzhou Road, Nanchang, 330006, Jiangxi, China. oralsurgdr@163.com.ORCID 0000-0002-4242-0682
Lan LiaoJiangxi Provincial Key Laboratory of Oral Biomedicine, Department of Oral Prosthodontics, the Affiliated Stomatological Hospital of Nanchang University, Nanchang, 330006, China. liaolan5106@163.com.
Jun WuJiangxi Provincial Key Laboratory of Oral Biomedicine, Department of Orthodontics, the Affiliated Stomatological Hospital of Nanchang University, Nanchang, 330006, China.
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe FOXP3/miR-146a/NF-κB axis was previously reported to modulate the induction and function of CD4+ Treg cells to alleviate oral lichen planus. Also, other signaling pathways including microRNA-155-IFN-γ loop and FOXP3/miR-146a/TRAF6 pathways were reported to be involved in the pathogenesis of oral lichen planus. In this study, we aimed to investigate the molecular mechanism underlying the pathogenesis of EOLP.

methodCircRNA microarray was used to observe the expression of candidate circRNAs in CD4+ T-cells collected from different groups. Real-time PCR and Western blot were conducted to observe the changes in the expression of different miRNAs, mRNAs and proteins. Flow cytometry was performed to compare the counts of Treg cells in the HC and EOLP groups, and ELISA was performed to evaluate the changes in the expression of inflammatory cytokines.

resultNo obvious differences were seen between the HC and EOLP groups in terms of age and gender. Among all candidate circRNAs, the expression of circ_003912 was most dramatically elevated in CD4+ T-cells collected from the EOLP group. The levels of miR-1231, miR-31, miR-647, FOXP3 mRNA and miR-146a were decreased while the expression of TRAF6 mRNA was increased in CD4+ T-cells collected from the EOLP group. The count of Treg cells in the EOLP group was dramatically increased. The levels of inflammatory cytokines including IL-4 IFN-γ, IL-10 and IL-2 were influenced by the presence of circ_003912. In CD4+ T-cells in the EOLP group, the levels of IL-4 and IL-10 were decreased while the levels of IFN-γ and IL-2 were increased. The presence of miR-1231, miR-31 and miR-647 all obviously inhibited the expression of circ_003912, which was validated to sponge the expression of above miRNAs. Also, FOXP3 mRNA was proved to be targeted by miR-1231, miR-31 and miR-647. Transfection of circ_003912 up-regulated the expression of circ_003912, miR-146a and FOXP3 mRNA/protein while down-regulating the expression of miR-1231, miR-31, miR-647, and TRAF6 mRNA/protein. The levels of inflammatory cytokines including IL-4 IFN-γ, IL-10 and IL-2 as well as the speed of cell proliferation were influenced by circ_003912.

conclusionIn this study, we investigated the molecular mechanisms underlying the pathogenesis of EOLP which involved the functioning of circ_003912. We first demonstrated that circ_003912 was up-regulated in CD4+ T-cells of the EOLP group. And miRNAs including miR-1231, miR-31 and miR-647 were sponged by circ_003912 and down-regulated in CD4+ T cells of the EOLP group, which subsequently up-regulated the expression of FOXP3 and miR-146a, and resulted in the inhibition of NF-kB.

Indexed as

AdultCD4-Positive T-LymphocytesCytokinesFemaleForkhead Transcription FactorsGene Expression RegulationHumansLichen Planus, OralMaleMicroRNAsMiddle AgedRNA, CircularRNA InterferenceRNA, MessengerSignal TransductionTHP-1 CellsCytokinesForkhead Transcription FactorsFOXP3 protein, humanMicroRNAsMIRN1231 microRNA, humanMIRN31 microRNA, humanMIRN647 microRNA, humanRNA, CircularRNA, MessengerCD4+ Treg cellscircRNAFOXP3miR-146aOral lichen planusTRAF6

Identifiers

PMID34670484
PMCPMC8527710
OpenAlexW3205649190

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.