ArticleNeurobiology of disease2014
DJ-1 ameliorates ischemic cell death in vitro possibly via mitochondrial pathway.
Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
The trial behind it
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Unconventional secretion of PARK7 requires lysosomal delivery via chaperone-mediated autophagy and specialized SNARE complex.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- DJ-1 interacts with the ectopic ATP-synthase in endothelial cells during acute ischemia and reperfusion.Scientific reports · 2022Article
- Biomarkers for Transient Ischemic Attack: A Brief Perspective of Current Reports and Future Horizons.Journal of clinical medicine · 2022Review
- DJ-1 administration exerts cardioprotection in a mouse model of acute myocardial infarction.Frontiers in pharmacology · 2022Article
- δ-Opioid Receptor Activation Attenuates the Oligomer Formation Induced by Hypoxia and/or α-Synuclein Overexpression/Mutation Through Dual Signaling Pathways.Molecular neurobiology · 2019Article
- p38 Inhibitor Protects Mitochondrial Dysfunction by Induction of DJ-1 Mitochondrial Translocation After Subarachnoid Hemorrhage.Journal of molecular neuroscience : MN · 2018Article
- Involvement of impaired autophagy and mitophagy in Neuro-2a cell damage under hypoxic and/or high-glucose conditions.Scientific reports · 2018Article
- 6-Hydroxydopamine induces secretion of PARK7/DJ-1 via autophagy-based unconventional secretory pathway.Autophagy · 2018Article
- 14,15-EET Suppresses Neuronal Apoptosis in Ischemia-Reperfusion Through the Mitochondrial Pathway.Neurochemical research · 2017Article
- 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 · 2017Review
- Intravenously Transplanted Human Bone Marrow Endothelial Progenitor Cells Engraft Within Brain Capillaries, Preserve Mitochondrial Morphology, and Display Pinocytotic Activity Toward Blood-Brain Barrier Repair in Ischemic Stroke Rats.Stem cells (Dayton, Ohio) · 2017Article
- Pretreatment with Sodium Phenylbutyrate Alleviates Cerebral Ischemia/Reperfusion Injury by Upregulating DJ-1 Protein.Frontiers in neurology · 2017Article
- Cyclosporine A Treatment Abrogates Ischemia-Induced Neuronal Cell Death by Preserving Mitochondrial Integrity through Upregulation of the Parkinson's Disease-Associated Protein DJ-1.CNS neuroscience & therapeutics · 2016Article
- Paracrine factors for neurodegenerative disorders: special emphasis on Parkinson's disease.Neural regeneration research · 2016Article
- Neural stem cells in Parkinson's disease: a role for neurogenesis defects in onset and progression.Cellular and molecular life sciences : CMLS · 2015Review
- The role of DJ-1 in the oxidative stress cell death cascade after stroke.Neural regeneration research · 2014Review
- Oxygen-glucose-deprived rat primary neural cells exhibit DJ-1 translocation into healthy mitochondria: a potent stroke therapeutic target.CNS neuroscience & therapeutics · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
DJ-1 is an important redox-reactive neuroprotective protein implicated in regulation of oxidative stress after ischemia. However the molecular mechanism, especially the mitochondrial function, by which DJ-1 protects neuronal 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 an in vitro model of stroke. Human neural progenitor cells (hNPCs) were initially exposed to oxygen-glucose deprivation and reperfusion injury, and thereafter, DJ-1 translocation was measured by immunocytochemistry and its secretion by hNPCs was detected by enzyme-linked immunosorbant assay (ELISA). Exposure of hNPCs to experimental stroke injury resulted in DJ-1 translocation into the mitochondria. Moreover, significant levels of DJ-1 protein were secreted by the injured hNPCs. Our findings revealed that DJ-1 principally participates in the early phase of stroke involving the mitochondrial pathway. DJ-1 was detected immediately after stroke and efficiently translocated into the mitochondria offering a new venue for developing treatment strategies against ischemic stroke.
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Registered trials
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.