Evidence map›Paper›PMID 27247192›Full record

ArticleCNS neuroscience & therapeutics2016

Cyclosporine A Treatment Abrogates Ischemia-Induced Neuronal Cell Death by Preserving Mitochondrial Integrity through Upregulation of the Parkinson's Disease-Associated Protein DJ-1.

Naoki Tajiri, Cesar V Borlongan, Yuji Kaneko

Open access · hybridAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Preclinical studies of mesenchymal stem cells transplantation in amyotrophic lateral sclerosis: a systemic review and metaanalysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Oxytocin modulates GABAScientific reports · 2016
    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

3 authors at 1 institution in 1 country.

Naoki TajiriCenter of Excellence for Aging & Brain Repair, Department of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, FL, USA.
Cesar V BorlonganCenter of Excellence for Aging & Brain Repair, Department of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, FL, USA.
Yuji KanekoCenter of Excellence for Aging & Brain Repair, Department of Neurosurgery and Brain Repair, University of South Florida Morsani College of Medicine, Tampa, FL, USA.
University of South Florida · US

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 R01 NS071956
6 · The paper itself

Abstract

aimsHypoxic-ischemia alters mitochondrial membrane potential (Δψm), respiratory-related enzymes, and mitochondrial DNA (mtDNA). Drugs acting on mitochondria, such as cyclosporine A (CsA), may reveal novel mitochondria-based cell death signaling targets for stroke. Our previous studies showed that Parkinson's disease-associated protein DJ-1 participates in the acute endogenous neuroprotection after stroke via mitochondrial pathway. DJ-1 was detected immediately after stroke and efficiently translocated into the mitochondria offering a new venue for developing treatment strategies against stroke. Here, we examined a molecular interaction between CsA and mitochondrial integrity in the in vitro acute stroke model of oxygen glucose deprivation/reperfusion (OGD/R) injury with emphasis on DJ-1.

methodsPrimary rat neuronal cells (PRNCs) were exposed to OGD/R injury and processed for immunocytochemistry, ELISA, and mitochondria-based molecular assays to reveal the role of DJ-1 in CsA modulation of mitochondrial integrity.

resultsAdministration of CsA before stroke onset (24 h pre-OGD/R) afforded significantly much more robust neuroprotective effects than when CsA was initiated after stroke (2 h post-OGD/R), revealing that CsA exerted neuroprotection in the early phase of ischemic stroke. CsA prevented the mitochondria-dependent cell death signaling pathway involved in cytochrome c (Cyt c)-induced intrinsic apoptotic process. CsA preserved cellular ATP content, but not hexokinase activity under hypoxic conditions. CsA prevented both mtDNA decrement and Δψm degradation after reperfusion, and enhanced secretion of DJ-1 in the mitochondria, coupled with reduced oxidative stress.

conclusionThese observations provided evidence that CsA maintained mitochondrial integrity likely via DJ-1 upregulation, supporting the concept that mitochondria-based treatments targeting the early phase of disease progression may prove beneficial in stroke.

Indexed as

Adenosine TriphosphateAnalysis of VarianceAnimalsCell SurvivalCerebral CortexCyclosporineCytochromes cDNA, MitochondrialDrug Administration ScheduleEmbryo, MammalianFluoresceinsGlucoseGlucose-6-PhosphateGlutathioneHypoxiaMembrane Potential, MitochondrialAdenosine Triphosphatecalcein AMCyclosporineCytochromes cDNA, MitochondrialFluoresceinsGlucoseGlucose-6-PhosphateGlutathionePARK7 protein, ratProtein Deglycase DJ-1Cytochrome cMitochondrial DNAMitochondrial membrane potential (Δψm)Mitochondrial permeability transition poreOxygen glucose deprivation/reperfusion injury

Identifiers

PMID27247192
PMCPMC5189675
OpenAlexW2414825922

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.