Evidence map›Paper›PMID 24382215›Full record

ArticleCNS neuroscience & therapeutics2014

Oxygen-glucose-deprived rat primary neural cells exhibit DJ-1 translocation into healthy mitochondria: a potent stroke therapeutic target.

Yuji Kaneko, Naoki Tajiri, Hideki Shojo, Cesar V Borlongan

Open access · hybridAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Potential biomarkers in hypoglycemic brain injury.Forensic science, medicine, and pathology · 2024
    Article
  2. Mitochondria in Cell-Based Therapy for Stroke.Antioxidants (Basel, Switzerland) · 2023
    Review
  3. Article
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Eye Opener in Stroke.Stroke · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Neuronal Preconditioning Requires the Mitophagic Activity of C-terminus of HSC70-Interacting Protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  14. Article
  15. Review
  16. Mechanisms of Parkinson's disease-related proteins in mediating secondary brain damage after cerebral ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Review
  17. Article
  18. Article
  19. Oxytocin modulates GABAScientific reports · 2016
    Article
  20. 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

4 authors at 2 institutions in 2 countries.

Yuji KanekoDepartment of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, FL, USA.
Naoki Tajiri
Hideki Shojo
Cesar V Borlongan
University of South Florida · USUniversity of Yamanashi · JP

Funding

Blood-Brain Barrier Repair in Cell Therapy for StrokeR01NS071956 · NINDS · UNIVERSITY OF SOUTH FLORIDA · PI BORLONGAN, CESARIO V, GARBUZOVA-DAVIS, SVITLANA NICOLAI · 2011 to 2015
$2.1M
NINDS NIH HHS 1R01NS071956-01NINDS NIH HHS R01 NS071956
6 · The paper itself

Abstract

aimsDJ-1 is a key redox-reactive neuroprotective protein implicated in regulation of oxidative stress after stroke. However, the molecular mechanism, especially the role of mitochondrial function, by which DJ-1 protects neural cells in stroke remains to be elucidated. The aim of this study was to reveal whether DJ-1 translocates into the mitochondria in exerting neuroprotection against oxidative stress. In particular, we examined DJ-1 secretion from primary rat neural cells (PRNCs) exposed to experimental stroke.

methodsPrimary rat neural cells were exposed to the oxygen-glucose deprivation (OGD), an established in vitro stroke model, and DJ-1 translocation was measured by immunocytochemistry, and its secretion detected by ELISA.

resultsUnder OGD, DJ-1 translocated into the healthy mitochondria, and significant levels of DJ-1 protein were detected. Treatment with anti-DJ-1 antibody reduced cell viability and mitochondrial activity, and increased glutathione level. Interestingly, OGD reversed the ratio of astrocyte/neuron cells (6/4 to 4/6).

conclusionsAltogether, these results revealed that DJ-1 participates in the acute endogenous neuroprotection after stroke via the mitochondrial pathway. That DJ-1 was detected immediately after stroke and efficiently translocated into the mitochondria offer a new venue for developing neuroprotective and/or neurorestorative strategies against ischemic stroke.

Indexed as

Analysis of VarianceAnimalsAstrocytesBrainCells, CulturedGlucoseHypoxiaMembrane Potential, MitochondrialMicrotubule-Associated ProteinsNeuronsOxidative StressProtein Deglycase DJ-1Protein TransportRatsGlucoseMicrotubule-Associated ProteinsPARK7 protein, ratProtein Deglycase DJ-1MitochondriaNeuroprotectionOxidative stressStem cellsStroke

Identifiers

PMID24382215
PMCPMC3947479
OpenAlexW2030844346

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.