Evidence map›Paper›PMID 35723715›Full record

ArticleOral health & preventive dentistry2022

Long Non-coding RNA PVT1 is Involved in the Pathological Mechanism of Pulpitis by Regulating miR-128-3p.

Lin Xia, Jian Wang, Yue Qi, Yongjie Fei, Dongmei Wang

Open access · greenAbstract read
In one paragraph

Article in Oral health & preventive dentistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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 23% 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, 12 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

5 authors.

Lin Xia
Jian Wang
Yue Qi
Yongjie Fei
Dongmei Wang

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposePulpitis is a common disease in stomatology, which is caused by dental pulp infection. It was found that long non-coding RNA regulates inflammation and repair responses through competitively sponging microRNAs. This study explored the expression and clinical significance of PVT1 in pulpitis patients, and further investigated the possible regulatory mechanism of PVT1 on pulpitis through in-vitro experiments. MATERIALS AND

methodsThe expression of PVT1 and miR-128-3p was detected through RT-qPCR. An ROC curve was drawn to estimate the diagnostic significance of PVT1 and miR-128-3p for pulpitis. An in-vitro pulpitis cell model was constructed to evaluate the effects of PVT1 or miR-128-3p on cell proliferation, apoptosis, and inflammatory response. The Luciferase reporter gene explored the interaction between PVT1 and miR-128-3p.

resultsThe expression of PVT1 increased, while the miR-128-3p level decreased, in the saliva of pulpitis patients. ROC curves showed that both PVT1 and miR-128-3p had the potential to diagnose pulpitis. This in-vitro study revealed that the expression of PVT1 was increased in the pulpitis cell model. A low level of PVT1 suppressed the hDPCs injury induced by LPS. The Luciferase reporter gene verified the targeting relationship between PVT1 and miR-128-3p, and the latter was negatively regulated by PVT1. Further in-vitro studies showed that inhibition of miR-128-3p could reverse the effect of si-PVT1 on cell viability, cell apoptosis and inflammatory response.

conclusionThis study revealed that knockdown of PVT1 may suppress the damage in pulpitis cell models induced by LPS via targeting miR-128-3p.

Indexed as

MicroRNAsPulpitisRNA, Long NoncodingCell ProliferationHumansLipopolysaccharidesLipopolysaccharidesMicroRNAsMIRN128 microRNA, humanRNA, Long NoncodingLPSmiR-128-3ppulpitisPVT1

Identifiers

PMID35723715
PMCPMC11641274
OpenAlexW4283211522

What OpenQuestion holds

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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.