ArticlePloS one2012
DJ-1 null dopaminergic neuronal cells exhibit defects in mitochondrial function and structure: involvement of mitochondrial complex I assembly.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mitochondrial Transfer in the Neurovascular Unit, Not Only for Energy Rescue: A Systematic Review.Aging and disease · 2024Pooled it
- Integrated Behavioral and Proteomic Characterization of MPPInternational journal of molecular sciences · 2025Article
- DJ-1 deficiency and aging: dual drivers of retinal mitochondrial dysfunction.bioRxiv : the preprint server for biology · 2025Article
- Mitochondrial Dysfunction in Genetic and Non-Genetic Parkinson's Disease.International journal of molecular sciences · 2025Review
- The Mitochondrial Foundations of Parkinson's Disease: Therapeutic Implications.Aging and disease · 2025Review
- Involvement of Mitochondria in Parkinson's Disease.International journal of molecular sciences · 2023Review
- Crif1 deficiency in dopamine neurons triggers early-onset parkinsonism.Molecular psychiatry · 2023Article
- Targeting Mitochondria as a Therapeutic Approach for Parkinson's Disease.Cellular and molecular neurobiology · 2023Review
- Molecular and Physiological Determinants of Amyotrophic Lateral Sclerosis: What the DJ-1 Protein Teaches Us.International journal of molecular sciences · 2023Review
- PARK7/DJ-1 in microglia: implications in Parkinson's disease and relevance as a therapeutic target.Journal of neuroinflammation · 2023Review
- Mitochondrial Bioenergy in Neurodegenerative Disease: Huntington and Parkinson.International journal of molecular sciences · 2023Review
- Depletion of dopamine in Parkinson's disease and relevant therapeutic options: A review of the literature.AIMS neuroscience · 2023Review
- Mitochondrial Respiratory Chain Supercomplexes: From Structure to Function.International journal of molecular sciences · 2022Review
- DJ-1 interacts with the ectopic ATP-synthase in endothelial cells during acute ischemia and reperfusion.Scientific reports · 2022Article
- Exploring therapeutic potential of mitophagy modulators usingFrontiers in aging neuroscience · 2022Review
- DJ-1 administration exerts cardioprotection in a mouse model of acute myocardial infarction.Frontiers in pharmacology · 2022Article
- Reappraisal of metabolic dysfunction in neurodegeneration: Focus on mitochondrial function and calcium signaling.Acta neuropathologica communications · 2021Review
- Cytoprotective Mechanisms of DJ-1: Implications in Cardiac Pathophysiology.Molecules (Basel, Switzerland) · 2021Review
- The roles of resveratrol on cardiac mitochondrial function in cardiac diseases.European journal of nutrition · 2021Review
- Mitochondria and Parkinson's Disease: Clinical, Molecular, and Translational Aspects.Journal of Parkinson's disease · 2021Review
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DJ-1 is a Parkinson's disease-associated gene whose protein product has a protective role in cellular homeostasis by removing cytosolic reactive oxygen species and maintaining mitochondrial function. However, it is not clear how DJ-1 regulates mitochondrial function and why mitochondrial dysfunction is induced by DJ-1 deficiency. In a previous study we showed that DJ-1 null dopaminergic neuronal cells exhibit defective mitochondrial respiratory chain complex I activity. In the present article we investigated the role of DJ-1 in complex I formation by using blue native-polyacrylamide gel electrophoresis and 2-dimensional gel analysis to assess native complex status. On the basis of these experiments, we concluded that DJ-1 null cells have a defect in the assembly of complex I. Concomitant with abnormal complex I formation, DJ-1 null cells show defective supercomplex formation. It is known that aberrant formation of the supercomplex impairs the flow of electrons through the channels between respiratory chain complexes, resulting in mitochondrial dysfunction. We took two approaches to study these mitochondrial defects. The first approach assessed the structural defect by using both confocal microscopy with MitoTracker staining and electron microscopy. The second approach assessed the functional defect by measuring ATP production, O(2) consumption, and mitochondrial membrane potential. Finally, we showed that the assembly defect as well as the structural and functional abnormalities in DJ-1 null cells could be reversed by adenovirus-mediated overexpression of DJ-1, demonstrating the specificity of DJ-1 on these mitochondrial properties. These mitochondrial defects induced by DJ-1mutation may be a pathological mechanism for the degeneration of dopaminergic neurons in Parkinson's disease.
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