Evidence map›Paper›PMID 31423743›Full record

ArticleCNS neuroscience & therapeutics2020

Corticosterone induces neurotoxicity in PC12 cells via disrupting autophagy flux mediated by AMPK/mTOR signaling.

Run-Dong Ma, Gui-Juan Zhou, Miao Qu, Ji-Hong Yi, Ya-Ling Tang, Xiang-Yi Yang, Ya-Xiong Nie, Hong-Feng Gu

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

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  13. Pharmaceuticals (Basel, Switzerland) · 2022
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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

8 authors at 2 institutions in 1 country.

Run-Dong MaDepartment of Neurology of the First Affiliated Hospital, University of South China, Hengyang, China.
Gui-Juan ZhouDepartment of Neurology of the First Affiliated Hospital, University of South China, Hengyang, China.
Miao QuDepartment of Physiology & Institute of Neuroscience, University of South China, Hengyang, China.
Ji-Hong YiInstitute of Neuroscience of the First Affiliated Hospital, University of South China, Hengyang, China.
Ya-Ling TangDepartment of Physiology & Institute of Neuroscience, University of South China, Hengyang, China.
Xiang-Yi YangDepartment of Neurology of the First Affiliated Hospital, University of South China, Hengyang, China.
Ya-Xiong NieDepartment of Neurology of the First Affiliated Hospital, University of South China, Hengyang, China.
Hong-Feng GuDepartment of Physiology & Institute of Neuroscience, University of South China, Hengyang, China.ORCID 0000-0002-4062-7057
First Affiliated Hospital of University of South China · CNUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsOur previous study indicated that chronic stress caused autophagy impairment and subsequent neuron apoptosis in hippocampus. However, the mechanism underlying the stress-induced damage to neurons is unclear. In present work, we investigated whether stress-level glucocorticoids (GCs) GCs promoted PC12 cell damage via AMPK/mTOR signaling-mediated autophagy.

methodsChronic stress-induced PC12 cell injury model was built by treatment with high level corticosterone (CORT). Cell injury was evaluated by flow cytometry assay and transmission electron microscopy observation.

resultsAutophagy flux was measured based on the changes in LC3-II and P62 protein expressions, and the color alteration of mCherry-GFP-LC3-II transfection. Our results showed that CORT not only increased cell injury and apoptosis, but also dysregulated AMPK/mTOR signaling-mediated autophagy flux, as indicated by the upregulated expression of LC3-II and P62 proteins, and the lowered ration of autolysosomes to autophagosomes. Mechanistically, our results demonstrated that autophagy activation by AMPK activator metformin or mTOR inhibitor rapamycin obviously promotes cell survival and autophagy flux, improved mitochondrial ultrastructure, and reduced expression of Cyt-C and caspase-3 in CORT-induced PC12 cells.

conclusionThese results indicate that high CORT triggers PC12 cell damage through disrupting AMPK/mTOR-mediated autophagy flux. Targeting this signaling may be a promising approach to protect against high CORT and chronic stress-induced neuronal impairment.

Indexed as

AMP-Activated Protein KinasesAnimalsApoptosisAutophagyCorticosteroneEnzyme ActivationFlow CytometryLysosomesMetforminMicrotubule-Associated ProteinsPC12 CellsPhagosomesRatsSignal TransductionSirolimusTOR Serine-Threonine KinasesAMP-Activated Protein KinasesAnxa3 protein, ratCorticosteroneMetforminMicrotubule-Associated ProteinsmTOR protein, ratSirolimusTOR Serine-Threonine KinasesAMPKautophagycorticosteronemTORneurotoxicity

Identifiers

PMID31423743
PMCPMC6978254
OpenAlexW2969531750

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.