ArticleJournal of neurotrauma2012
Mitochondrial injury after mechanical stretch of cortical neurons in vitro: biomarkers of apoptosis and selective peroxidation of anionic phospholipids.
Article in Journal of neurotrauma, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Exploratory Characterization of Adaptive Eye Strategies to High-Acceleration Loading in the Great Spotted Woodpecker.Annals of biomedical engineering · 2026Article
- Temperature induces brain-intake shift of recombinant high-density lipoprotein after traumatic brain injury.Journal of nanobiotechnology · 2024Article
- Transforming growth factor-β1 protects mechanically injured cortical murine neurons by reducing trauma-induced autophagy and apoptosis.Frontiers in cellular neuroscience · 2024Article
- Pannexin-1 opening in neuronal edema causes cell death but also leads to protection via increased microglia contacts.Cell reports · 2023Article
- Lower and higher volumes of physical exercise build up brain reserves against memory deficits triggered by a head injury in mice.Experimental neurology · 2023Article
- Fetuin-A alleviates neuroinflammation against traumatic brain injury-induced microglial necroptosis by regulating Nrf-2/HO-1 pathway.Journal of neuroinflammation · 2022Article
- Lupeol Treatment Attenuates Activation of Glial Cells and Oxidative-Stress-Mediated Neuropathology in Mouse Model of Traumatic Brain Injury.International journal of molecular sciences · 2022Article
- A Brief Review of In Vitro Models for Injury and Regeneration in the Peripheral Nervous System.International journal of molecular sciences · 2022Review
- Prokineticin-2 prevents neuronal cell deaths in a model of traumatic brain injury.Nature communications · 2021Observational
- Assessment of the Effects of Stretch-Injury on Primary Rat Microglia.Molecular neurobiology · 2021Article
- Seawater Immersion Aggravates Early Mitochondrial Dysfunction and Increases Neuronal Apoptosis After Traumatic Brain Injury.Cellular and molecular neurobiology · 2020Article
- Mechanical regulation of oligodendrocyte biology.Neuroscience letters · 2020Review
- Redox Epiphospholipidome in Programmed Cell Death Signaling: Catalytic Mechanisms and Regulation.Frontiers in endocrinology · 2020Review
- Review
- Testosterone Administration after Traumatic Brain Injury Reduces Mitochondrial Dysfunction and Neurodegeneration.Journal of neurotrauma · 2019Article
- Cardiolipin-Dependent Mitophagy Guides Outcome after Traumatic Brain Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Disentangling oxidation/hydrolysis reactions of brain mitochondrial cardiolipins in pathogenesis of traumatic injury.JCI insight · 2018Article
- Effect of high fat diet on phenotype, brain transcriptome and lipidome in Alzheimer's model mice.Scientific reports · 2017Article
- Probenecid and N-Acetylcysteine Prevent Loss of Intracellular Glutathione and Inhibit Neuronal Death after Mechanical Stretch Injury In Vitro.Journal of neurotrauma · 2016Article
- Therapies targeting lipid peroxidation in traumatic brain injury.Brain research · 2016Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Mechanical injury of neurites accompanied by rupture of mitochondrial membranes may lead to immediate nonspecific release and spreading of pro-apoptotic factors and activation of proteases, that is, execution of apoptotic program. In the current work, we studied the time course of the major biomarkers of apoptosis as they are induced by exposure of rat cortical neurons to mechanical stretch. By using transmission electron microscopy, we found that mitochondria in the neurites were damaged early (1 h) after mechanical stretch injury whereas somal mitochondria were significantly more resistant and demonstrated structural damage and degenerative mitochondrial changes at a later time point after stretch (12 h). We also report that the stretch injury caused immediate activation of reactive oxygen species production followed by selective oxidation of a mitochondria-specific phospholipid, cardiolipin, whose individual peroxidized molecular species have been identified and quantified by electrospray ionization mass spectrometry analysis. Most abundant neuronal phospholipids - phosphatidylcholine, phophatidylethanolamine - did not undergo oxidative modification. Simultaneously, a small-scale release of cytochrome c was observed. Notably, caspase activation and phosphatidylserine externalization - two irreversible apoptotic events designating a point of no return - are substantially delayed and do not occur until 6-12 h after the initial impact. The early onset of reactive oxygen species production and cytochrome c release may be relevant to direct stretch-induced damage to mitochondria. The delayed emergence of apoptotic neuronal death after the immediate mechanical damage to mitochondria suggests a possible window of opportunity for targeted therapies.
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