Evidence map›Paper›PMID 32188458›Full record

ArticleJournal of nanobiotechnology2020

The interrupted effect of autophagic flux and lysosomal function induced by graphene oxide in p62-dependent apoptosis of F98 cells.

Chao Zhang, Xiaoli Feng, Longwen He, Yaqing Zhang, Longquan Shao

Open access · goldAbstract read
In one paragraph

Article in Journal of nanobiotechnology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 47 citations in OpenAlex.

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  13. Micro- and Nanosized Substances Cause Different Autophagy-Related Responses.International journal of molecular sciences · 2021
    Review
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

5 authors at 2 institutions in 1 country.

Chao ZhangStomatological Hospital, Southern Medical University (Guangdong Provincial Stomatological Hospital), Guangzhou, 510280, China.
Xiaoli FengStomatological Hospital, Southern Medical University (Guangdong Provincial Stomatological Hospital), Guangzhou, 510280, China.
Longwen HeStomatological Hospital, Southern Medical University (Guangdong Provincial Stomatological Hospital), Guangzhou, 510280, China.
Yaqing ZhangStomatological Hospital, Southern Medical University (Guangdong Provincial Stomatological Hospital), Guangzhou, 510280, China.
Longquan ShaoStomatological Hospital, Southern Medical University (Guangdong Provincial Stomatological Hospital), Guangzhou, 510280, China. shaolongquan@smu.edu.cn.
Guangdong Province Stomatological Hospital · CNSouthern Medical University · CN

Funding

National Natural Science Foundation of China 81801007Natural Science Foundation of Guangdong Province 2018A030310442Postdoctoral Science Foundation of China 2019M652980Science and Cultivation Foundation of Stomatological Hospital of Southern Medical University PY2018027
6 · The paper itself

Abstract

backgroundGraphene oxide (GO) nanoparticles (NPs) have been widely applied in various fields, especially in biomedical applications. Extensive studies have suggested that GO can pass through the blood-brain barrier (BBB) and induce abnormal autophagy and cytotoxicity in the central nervous system (CNS). However, the effect and specific mechanism of GO on astrocytes, the most abundant cells in the brain still has not been extensively investigated.

resultsIn this study, we systematically explored the toxicity and mechanism of GO exposure in the rat astroglioma-derived F98 cell line using molecular biological techniques (immunofluorescence staining, flow cytometry and Western blot) at the subcellular level and the signaling pathway level. Cells exposed to GO exhibited decreased cell viability and increased lactate dehydrogenase (LDH) release in a concentration- and time-dependent manner. GO-induced autophagy was evidenced by transmission electron microscopy (TEM) and immunofluorescence staining. Western blots showed that LC3II/I and p62 were upregulated and PI3K/Akt/mTOR was downregulated. Detection of lysosomal acidity and cathepsin B activity assay indicated the impairment of lysosomal function. Annexin V-FITC-PI detection showed the occurrence of apoptosis after GO exposure. The decrease in mitochondrial membrane potential (MMP) with an accompanying upregulation of cleaved caspase-3 and Bax/Bcl-2 further suggested that endogenous signaling pathways were involved in GO-induced apoptosis.

conclusionThe exposure of F98 cells to GO can elicit concentration- and time-dependent toxicological effects. Additionally, increased autophagic response can be triggered after GO treatment and that the blocking of autophagy flux plays a vital role in GO cytotoxicity, which was determined to be related to dysfunction of lysosomal degradation. Importantly, the abnormal accumulation of autophagic substrate p62 protein can induce capase-3-mediated apoptosis. Inhibition of abnormal accumulation of autophagic cargo could alleviate the occurrence of GO-induced apoptosis in F98 cells.

Indexed as

AnimalsAnnexinsApoptosisAstrocytesAutophagyCaspase 3Cell AdhesionCell Line, TumorCell SurvivalGraphiteLysosomesMembrane Potential, MitochondrialNanoparticlesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-bcl-2RatsAnnexinsCaspase 3graphene oxideGraphitePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-bcl-2TOR Serine-Threonine KinasesApoptosisAstrocyteAutophagyGraphene oxidep62

Identifiers

PMID32188458
PMCPMC7081710
OpenAlexW3011894766

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.