Evidence map›Paper›PMID 26760769›Full record

ArticleOncotarget2016

Epigallocatechin-3-gallate induces oxidative phosphorylation by activating cytochrome c oxidase in human cultured neurons and astrocytes.

Gloria Castellano-González, Nicolas Pichaud, J William O Ballard, Alban Bessede, Helder Marcal, Gilles J Guillemin

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 41 citations in OpenAlex.

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  18. Neuroprotective Role of Phytochemicals.Molecules (Basel, Switzerland) · 2018
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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 3 institutions in 2 countries.

Gloria Castellano-GonzálezMND and Neurodegenerative Diseases Research Group, Australian School of Advanced Medicine (ASAM), Macquarie University, Sydney, Australia.
Nicolas PichaudDepartment of Biological and Environmental Sciences, University of Gothenburg, Göteborg, Sweden.
J William O BallardSchool of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, Australia.
Alban BessedeImmusmol Pty Ltd., Pessac, France.
Helder MarcalTopical Therapeutics Research Group, School of Medical Sciences, The University of New South Wales, Sydney, Australia.
Gilles J GuilleminMND and Neurodegenerative Diseases Research Group, Australian School of Advanced Medicine (ASAM), Macquarie University, Sydney, Australia.
Macquarie University · AUUNSW Sydney · AUUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction and resulting energy impairment have been identified as features of many neurodegenerative diseases. Whether this energy impairment is the cause of the disease or the consequence of preceding impairment(s) is still under discussion, however a recovery of cellular bioenergetics would plausibly prevent or improve the pathology. In this study, we screened different natural molecules for their ability to increase intracellular adenine triphosphate purine (ATP). Among them, epigallocatechin-3-gallate (EGCG), a polyphenol from green tea, presented the most striking results. We found that it increases ATP production in both human cultured astrocytes and neurons with different kinetic parameters and without toxicity. Specifically, we showed that oxidative phosphorylation in human cultured astrocytes and neurons increased at the level of the routine respiration on the cells pre-treated with the natural molecule. Furthermore, EGCG-induced ATP production was only blocked by sodium azide (NaN3) and oligomycin, inhibitors of cytochrome c oxidase (CcO; complex IV) and ATP synthase (complex V) respectively. These findings suggest that the EGCG modulates CcO activity, as confirmed by its enzymatic activity. CcO is known to be regulated differently in neurons and astrocytes. Accordingly, EGCG treatment is acting differently on the kinetic parameters of the two cell types. To our knowledge, this is the first study showing that EGCG promotes CcO activity in human cultured neurons and astrocytes. Considering that CcO dysfunction has been reported in patients having neurodegenerative diseases such as Alzheimer's disease (AD), we therefore suggest that EGCG could restore mitochondrial function and prevent subsequent loss of synaptic function.

Indexed as

Adenosine TriphosphateAstrocytesBlotting, WesternBrainCatechinCell ProliferationCell RespirationCells, CulturedElectron Transport Complex IVFetusHumansMembrane Potential, MitochondrialMitochondriaNeuronsNeuroprotective AgentsOxidation-ReductionAdenosine TriphosphateCatechinElectron Transport Complex IVepigallocatechin gallateNeuroprotective AgentsRNA, MessengerATPcytochrome c oxidaseepigallocatechin-3-gallateGerotargetmitochondrianeurodegeneration

Identifiers

PMID26760769
PMCPMC4884929
OpenAlexW2239917206

What OpenQuestion holds

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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.