ArticleNeurotoxicity research2013
α-Synuclein protects neurons from apoptosis downstream of free-radical production through modulation of the MAPK signalling pathway.
Article in Neurotoxicity research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Therapeutic Potential of αS Evolvability for Neuropathic Gaucher Disease.Biomolecules · 2021Article
- Therapeutic Potential ofParkinson's disease · 2021Review
- Protective role of renal proximal tubular alpha-synuclein in the pathogenesis of kidney fibrosis.Nature communications · 2020Article
- Surgery, Anesthesia and Intensive Care Environment Induce Delirium-Like Behaviors and Impairment of Synaptic Function-Related Gene Expression in Aged Mice.Frontiers in aging neuroscience · 2020Article
- Protective Effects of 6-(Methylsulfinyl)hexyl Isothiocyanate on AβInternational journal of molecular sciences · 2018Article
- Article
- MiR-19b alleviates MPPRSC advances · 2018Article
- Mitochondria and α-Synuclein: Friends or Foes in the Pathogenesis of Parkinson's Disease?Genes · 2017Review
- Autophagy enhancement is rendered ineffective in presence of α-synuclein in melanoma cells.Journal of cell communication and signaling · 2017Article
- Age-dependent alpha-synuclein accumulation is correlated with elevation of mitochondrial TRPC3 in the brains of monkeys and mice.Journal of neural transmission (Vienna, Austria : 1996) · 2017Article
- Alpha-synuclein prevents the formation of spherical mitochondria and apoptosis under oxidative stress.Scientific reports · 2017Article
- Role of cytochrome c in α-synuclein radical formation: implications of α-synuclein in neuronal death in Maneb- and paraquat-induced model of Parkinson's disease.Molecular neurodegeneration · 2016Article
- Convergence of Parkin, PINK1, and α-Synuclein on Stress-induced Mitochondrial Morphological Remodeling.The Journal of biological chemistry · 2015Article
- Article
- Genetic risk prediction and neurobiological understanding of alcoholism.Translational psychiatry · 2014Article
- α-Synuclein and mitochondria: partners in crime?Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013Review
- Effect of α-synuclein on amyloid β-induced toxicity: relevance to Lewy body variant of Alzheimer disease.Neurochemical research · 2013Article
- Rotenone upregulates alpha-synuclein and myocyte enhancer factor 2D independently from lysosomal degradation inhibition.BioMed research international · 2013Article
- Early Alzheimer's and Parkinson's disease pathology in urban children: Friend versus Foe responses--it is time to face the evidence.BioMed research international · 2013Review
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3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
α-Synuclein is a pre-synaptic chaperone and its accumulation contributes to differential cell loss in Parkinson's disease. Cytoplasmic expression of α-synuclein can directly modulate apoptotic pathways and contribute to cell survival, whereas induced over-expression of the protein causes oxidative stress through mitochondrial and cytosolic free-radical production. This study aimed to clarify the contribution of endogenous α-synuclein to oxidative stress and its association with cell death. Primary cortical neurons were derived from α-synuclein knock-out (Snca-/-) and wild-type (C57BL/6; WT) mice and treated with in vitro models of oxidative-stress, complex I inhibition and excitotoxicity. Mitochondrial free radical production was determined in isolated mitochondria derived from each mouse strain. Snca-/- derived cortical cultures were more susceptible (P < 0.05) to oxidative-stress, but not excitotoxicity. This result was determined by significant increases in cell death (Propidium-Iodide staining) after 6 h treatment in Snca-/- (45 % ± 2.7 SEM), relative to WT (33 % ± 3.9 SEM) cultures. α-Synuclein also confers significant (P < 0.05) resistance to low-dose (5 nM) rotenone toxicity, with a twofold reduction in cell death in WT, compared with Snca-/- cortical neurons. The expression of α-synuclein had no effect on cortical glutathione levels, or the production of reactive oxygen intermediates in isolated mitochondria. These data indicate that endogenous levels of α-synuclein confer resistance to oxidative stress downstream of free radical production and scavenging. The current data suggest that α-synuclein prevents cytochrome c release and apoptosis through inhibition of the MAPK signalling pathway.
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