Evidence map›Paper›PMID 30150770›Full record

ArticleScientific reports2018

Acetylation state of RelA modulated by epigenetic drugs prolongs survival and induces a neuroprotective effect on ALS murine model.

Lorenzo Schiaffino, Roberta Bonafede, Ilaria Scambi, Edoardo Parrella, Marina Pizzi, Raffaella Mariotti

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

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  18. Mitigation of ALS Pathology by Neuron-Specific Inhibition of Nuclear Factor Kappa B Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
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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.

Lorenzo SchiaffinoDepartment of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.
Roberta BonafedeDepartment of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.
Ilaria ScambiDepartment of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.
Edoardo ParrellaDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Marina PizziDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Raffaella MariottiDepartment of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy. raffaella.mariotti@univr.it.
University of Verona · ITUniversity of Brescia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation in acetylation homeostasis has been implicated in the pathogenesis of the amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder. It is known that the acetylation of transcriptional factors regulates their activity. The acetylation state of NF-kB RelA has been found to dictate the neuroprotective versus the neurotoxic effect of p50/RelA. Here we showed that the pro-apoptotic acetylation mode of RelA, involving a general lysine deacetylation of the subunit with the exclusion of the lysine 310, is evident in the lumbar spinal cord of SOD1(G93A) mice, a murine model of ALS. The administration of the HDAC inhibitor MS-275 and the AMPK/sirtuin 1 activator resveratrol restored the normal RelA acetylation in SOD1(G93A) mice. The SOD1(G93A) mice displayed a 3 weeks delay of the disease onset, associated with improvement of motor performance, and 2 weeks increase of lifespan. The epigenetic treatment rescued the lumbar motor neurons affected in SOD1(G93A) mice, accompanied by increased levels of protein products of NF-kB-target genes, Bcl-xL and brain-derived neurotrophic factor. In conclusion, we here demonstrate that MS-275 and resveratrol restore the acetylation state of RelA in the spinal cord, delaying the onset and increasing the lifespan of SOD1(G93A) mice.

Indexed as

AcetylationAmyotrophic Lateral SclerosisAnimalsBiomarkersDisease Models, AnimalEpigenesis, GeneticHistonesMiceMotor NeuronsNeurodegenerative DiseasesNeuroprotective AgentsPrognosisResveratrolSignal TransductionSpinal CordSuperoxide DismutaseBiomarkersHistonesNeuroprotective AgentsResveratrolSuperoxide DismutaseTranscription Factor RelA

Identifiers

PMID30150770
PMCPMC6110772
OpenAlexW2888564965

What OpenQuestion holds

Textmetadata
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.