Evidence map›Paper›PMID 32781723›Full record

ArticleMaterials (Basel, Switzerland)2020

Bioenergetic Impairment of Triethylene Glycol Dimethacrylate- (TEGDMA-) Treated Dental Pulp Stem Cells (DPSCs) and Isolated Brain Mitochondria are Amended by Redox Compound Methylene Blue

Krisztina Mikulás, Timea Komlódi, Anna Földes, Gergely Sváb, Gergő Horváth, Ádám Miklós Nagy, Attila Ambrus, Szabolcs Gyulai-Gaál, István Gera, Péter Hermann and 2 more

Open access · goldAbstract read
In one paragraph

Article in Materials (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 43% 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

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
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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

12 authors at 1 institution in 2 countries.

Krisztina MikulásDepartment of Prosthodontics, Semmelweis University, 1088 Budapest, Hungary.
Timea KomlódiDepartment of Medical Biochemistry, MTA-SE, Laboratory of Neurobiochemistry, Semmelweis University, 1094 Budapest, Hungary.
Anna FöldesDepartment of Oral Biology, Semmelweis University, 1089 Budapest, Hungary.ORCID 0000-0002-4182-7886
Gergely SvábDepartment of Medical Biochemistry, MTA-SE, Laboratory of Neurobiochemistry, Semmelweis University, 1094 Budapest, Hungary.
Gergő HorváthDepartment of Medical Biochemistry, MTA-SE, Laboratory of Neurobiochemistry, Semmelweis University, 1094 Budapest, Hungary.ORCID 0000-0001-5386-9509
Ádám Miklós NagyDepartment of Medical Biochemistry, MTA-SE, Laboratory of Neurobiochemistry, Semmelweis University, 1094 Budapest, Hungary.ORCID 0000-0002-9568-2555
Attila AmbrusDepartment of Medical Biochemistry, MTA-SE, Laboratory of Neurobiochemistry, Semmelweis University, 1094 Budapest, Hungary.
Szabolcs Gyulai-GaálDepartment of Oral Diagnostics, Semmelweis University, 1088 Budapest, Hungary.
István GeraDepartment of Periodontology, Semmelweis University, 1088 Budapest, Hungary.
Péter HermannDepartment of Prosthodontics, Semmelweis University, 1088 Budapest, Hungary.
Gábor VargaDepartment of Oral Biology, Semmelweis University, 1089 Budapest, Hungary.
László TretterDepartment of Medical Biochemistry, MTA-SE, Laboratory of Neurobiochemistry, Semmelweis University, 1094 Budapest, Hungary.
Semmelweis University · HU

Funding

Hungarian Academy of Sciences MTA TKI 02001Hungarian Brain Research Program KTIA_13_NAP-A-III/6 and 2017-1.2.1-NKP-2017-00002Hungarian Human Resources Development Operational Program EFOP-3.6.2-16-2017-00006Hungarian Scientific Research Fund NK112230
6 · The paper itself

Abstract

backgroundTriethylene glycol dimethacrylate (TEGDMA) monomers released from resin matrix are toxic to dental pulp cells, induce apoptosis, oxidative stress and decrease viability. Recently, mitochondrial complex I (CI) was identified as a potential target of TEGDMA. In isolated mitochondria supported by CI, substrates oxidation and ATP synthesis were inhibited, reactive oxygen species production was stimulated. Contrary to that, respiratory Complex II was not impaired by TEGDMA. The beneficial effects of electron carrier compound methylene blue (MB) are proven in many disease models where mitochondrial involvement has been detected. In the present study, the bioenergetic effects of MB on TEGDMA-treated isolated mitochondria and on human dental pulp stem cells (DPSC) were analyzed.

methodsIsolated mitochondria and DPSC were acutely exposed to low millimolar concentrations of TEGDMA and 2 μM concentration of MB. Mitochondrial and cellular respiration and glycolytic flux were measured by high resolution respirometry and by Seahorse XF extracellular analyzer. Mitochondrial membrane potential was measured fluorimetrically.

resultsMB partially restored the mitochondrial oxidation, rescued membrane potential in isolated mitochondria and significantly increased the impaired cellular O

conclusionMB is able to protect against TEGDMA-induced CI damage, and might provide protective effects in resin monomer exposed cells.

Indexed as

DPSCmethylene bluemitochondriaoxygen consumptionTEGDMA

Identifiers

PMID32781723
PMCPMC7475988
OpenAlexW3047020485

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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.