Evidence map›Paper›PMID 25467236›Full record

ArticleClinical oral investigations2015

NADPH oxidase 4 is involved in the triethylene glycol dimethacrylate-induced reactive oxygen species and apoptosis in human embryonic palatal mesenchymal and dental pulp cells.

Cheng-Chang Yeh, Jenny Zwei-Chieng Chang, Wan-Hsien Yang, Hao-Hueng Chang, Eddie Hsiang-Hua Lai, Mark Yen-Ping Kuo

Abstract read
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Article in Clinical oral investigations, 2015. 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
1.2field-weighted citation impact, top 25% 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.

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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

6 authors at 2 institutions in 1 country.

Cheng-Chang YehSchool of Dentistry, College of Medicine and Department of Dentistry, National Taiwan University Hospital, National Taiwan University Medical Center, 1 Chang-Te Street, Taipei, 10048, Taiwan.
Jenny Zwei-Chieng Chang
Wan-Hsien Yang
Hao-Hueng Chang
Eddie Hsiang-Hua Lai
Mark Yen-Ping Kuo
National Taiwan University · TWNational Taiwan University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTriethylene glycol dimethacrylate (TEGDMA) is a common component of resin-based dental composites and endodontic sealers. TEGDMA induces apoptosis in several types of cells. However, the mechanisms are not completely understood. The aim of this study was to investigate the mechanisms underlying TEGDMA-induced apoptosis in human embryonic palatal mesenchymal (HEPM) pre-osteoblasts and primary human dental pulp (HDP) cells. MATERIAL AND

methodsCell viability was examined after TEGDMA treatment. Cell cycle progression was checked by flow cytometry. Apoptotic cells were evaluated using terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling assay and visualized by fluorescence microscopy. Western blot analyses were performed to determine expressions of apoptosis-related proteins. The production of reactive oxygen species (ROS) was detected using flow cytometry. NADPH oxidase 4 (NOX4) expression levels were investigated using real-time quantitative polymerase chain reaction and Western blot analyses.

resultsTEGDMA increased cytosol cytochrome c levels and activated caspase-9 in HEPM and HDP cells. TEGDMA decreased the expression of anti-apoptotic protein Bcl-XL. TEGDMA-induced apoptosis was inhibited by caspase-9-specific inhibitor, anti-oxidants, NOX inhibitor, NOX4 inhibitor, and NOX4 small interfering RNA (siRNA). TEGDMA increased ROS production and upregulated NOX4 mRNA and protein expression. TEGDMA-induced intracellular ROS production was inhibited by NOX inhibitor and NOX4 inhibitor.

conclusionsWe demonstrate significant involvement of NOX4 in the TEGDMA-induced ROS. NOX4-derived ROS subsequently induces mitochondrial cytochrome c release leading to apoptosis through activation of the intrinsic apoptotic pathway. CLINICAL RELEVANCE: NOX4 may be a potential target for strategies to prevent or ameliorate the TEGDMA-induced toxicity in HEPM and HDP cells.

Indexed as

ApoptosisBlotting, WesternCell CycleCell SurvivalDental PulpFlow CytometryHumansIn Situ Nick-End LabelingNADPH Oxidase 4OsteoblastsPalatePolyethylene GlycolsPolymethacrylic AcidsReactive Oxygen SpeciesReal-Time Polymerase Chain ReactionNADPH Oxidase 4Polyethylene GlycolsPolymethacrylic AcidsReactive Oxygen Speciestriethylene glycol dimethacrylate

Identifiers

PMID25467236
OpenAlexW1991322109

What OpenQuestion holds

Textmetadata
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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.