ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Declines in Drp1 and parkin expression underlie DNA damage-induced changes in mitochondrial length and neuronal death.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 54 citations in OpenAlex.
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- Interrogating the Etiology of Sporadic Alzheimer's Disease Using Aging Rhesus Macaques: Cellular, Molecular, and Cortical Circuitry Perspectives.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
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- Drp1 regulates transcription of ribosomal protein genes in embryonic hearts.Journal of cell science · 2022Article
- PERK Pathway and Neurodegenerative Disease: To Inhibit or to Activate?Biomolecules · 2021Review
- Mitochondrial Behavior in Axon Degeneration and Regeneration.Frontiers in aging neuroscience · 2021Review
- Intracellular delivery of Parkin rescues neurons from accumulation of damaged mitochondria and pathological α-synuclein.Science advances · 2020Article
- Tenofovir disoproxil fumarate induces peripheral neuropathy and alters inflammation and mitochondrial biogenesis in the brains of mice.Scientific reports · 2019Article
- Mitochondrial biogenesis is altered in HIV+ brains exposed to ART: Implications for therapeutic targeting of astroglia.Neurobiology of disease · 2019Article
- Stress-induced phospho-ubiquitin formation causes parkin degradation.Scientific reports · 2019Article
- Nuclear factor (erythroid-derived 2)-like 2 antioxidative response mitigates cytoplasmic radiation-induced DNA double-strand breaks.Cancer science · 2019Article
- ROS as Regulators of Mitochondrial Dynamics in Neurons.Cellular and molecular neurobiology · 2018Review
- Guanabenz promotes neuronal survival via enhancement of ATF4 and parkin expression in models of Parkinson disease.Experimental neurology · 2018Article
- Mdivi-1 pretreatment mitigates isoflurane-induced cognitive deficits in developmental rats.American journal of translational research · 2018Article
- Parkin Overexpression Ameliorates PrP106-126-Induced Neurotoxicity via Enhanced Autophagy in N2a Cells.Cellular and molecular neurobiology · 2017Article
- A novel role for endothelial tetrahydrobiopterin in mitochondrial redox balance.Free radical biology & medicine · 2017Article
- Ultrastructural evidence for impaired mitochondrial fission in the aged rhesus monkey dorsolateral prefrontal cortex.Neurobiology of aging · 2017Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Maintaining proper mitochondrial length is essential for normal mitochondrial function in neurons. Mitochondrial fragmentation has been associated with neuronal cell death caused by a variety of experimental toxic stressors. Despite the fact that oxidative stress is a hallmark of neurodegenerative conditions and aging and the resulting activation of p53 is believed to contribute to the neuropathology, little is still known regarding changes in mitochondrial morphology in p53-dependent neuronal death. Therefore, we specifically addressed the relationship between genotoxic stress, p53 activation, and the regulation of mitochondrial morphology in neurons. In cultured postnatal mouse cortical neurons, treatment with the DNA-damaging agent camptothecin (CPT) resulted in elongated mitochondria, in contrast to fragmented mitochondria observed upon staurosporine and glutamate treatment. In fibroblasts, however, CPT resulted in fragmented mitochondria. CPT treatment in neurons suppressed expression of the mitochondrial fission protein Drp1 and the E3 ubiquitin ligase parkin. The presence of elongated mitochondria and the declines in Drp1 and parkin expression occurred before the commitment point for apoptosis. The CPT-induced changes in Drp1 and parkin were not observed in p53-deficient neurons, while p53 overexpression alone was sufficient to reduce the expression of the two proteins. Elevating Drp1 or parkin expression before CPT treatment enhanced neuronal viability and restored a normal pattern of mitochondrial morphology. The present findings demonstrate that genotoxic stress in neurons results in elongated mitochondria in contrast to fission induced by other forms of stress, and p53-dependent declines in Drp1 and parkin levels contribute to altered mitochondrial morphology and cell death.
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