Evidence map›Paper›PMID 30888577›Full record

ArticleNeurochemical research2019

Mitochondrial Dynamics Impairment in Dexamethasone-Treated Neuronal Cells.

Wilasinee Suwanjang, Kay L H Wu, Supaluk Prachayasittikul, Banthit Chetsawang, Komgrid Charngkaew

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
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 3 institutions in 2 countries.

Wilasinee SuwanjangCenter for Research and Innovation, Faculty of Medical Technology, Mahidol University, 10700, Bangkok, Thailand. wilasinee.suw@mahidol.ac.th.
Kay L H WuInstitute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, 83301, Taiwan, Republic of China.
Supaluk PrachayasittikulCenter of Data Mining and Biomedical Informatics, Faculty of Medical Technology, Mahidol University, 10700, Bangkok, Thailand.
Banthit ChetsawangResearch Center for Neuroscience, Institute of Molecular Biosciences, Mahidol University, 73170, Nakhonpathom, Thailand.
Komgrid CharngkaewDepartment of Pathology, Faculty of Medicine, Siriraj Hospital, 10700, Bangkok, Thailand.
Mahidol University · THKaohsiung Chang Gung Memorial Hospital · TWSiriraj Hospital · TH

Funding

Mahidol University and the Thailand Research Fund (TRF) under a research grant for new scholar MRG5980032The Committee for Aid and Education in Neurochemistry of the International Society for Neurochemistry and Chang Gung Medical Foundation OMRPG8C0021
6 · The paper itself

Abstract

Dexamethasone is an approved steroid for clinical use to activate or suppress cytokines, chemokines, inflammatory enzymes and adhesion molecules. It enters the brain, by-passing the blood brain barrier, and acts through genomic mechanisms. High levels of dexamethasone are able to induce neuronal cell loss, reduce neurogenesis and cause neuronal dysfunction. The exact mechanisms of steroid, especially the dexamethasone contribute to neuronal damage remain unclear. Therefore, the present study explored the mitochondrial dynamics underlying dexamethasone-induced toxicity of human neuroblastoma SH-SY5Y cells. Neuronal cells treatment with the dexamethasone resulted in a marked decrease in cell proliferation. Dexamethasone-induced neurotoxicity also caused upregulation of mitochondrial fusion and cleaved caspase-3 proteins expression. Mitochondria fusion was found in large proportions of dexamethasone-treated cells. These results suggest that dexamethasone-induced hyperfused mitochondrial structures are associated with a caspase-dependent death process in dexamethasone-induced neurotoxicity. These findings point to the high dosage of dexamethasone as being neurotoxic through impairment of mitochondrial dynamics.

Indexed as

Adenosine TriphosphateCaspase 3Cell Line, TumorCell ProliferationDexamethasoneDynaminsGTP PhosphohydrolasesHumansMicrotubule-Associated ProteinsMitochondriaMitochondrial DynamicsMitochondrial ProteinsNeuronsProtein KinasesPTEN-Induced Putative KinaseReactive Oxygen SpeciesAdenosine TriphosphateCASP3 protein, humanCaspase 3DexamethasoneDNM1L protein, humanDynaminsGTP PhosphohydrolasesMicrotubule-Associated ProteinsMitochondrial Proteinsparkin proteinProtein KinasesPTEN-Induced Putative KinaseReactive Oxygen SpeciesRNA, MessengerUbiquitin-Protein LigasesCell DeathDexamethasoneMitochondrial dynamicsMitophagyNeuron

Identifiers

PMID30888577
OpenAlexW2923553999

What OpenQuestion holds

Textmetadata
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.