ArticleNeurotoxicology2014
Mechanical stretch exacerbates the cell death in SH-SY5Y cells exposed to paraquat: mitochondrial dysfunction and oxidative stress.
Article in Neurotoxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Immune regulation and cellular crosstalk drive non-fibrotic lung remodeling in pre-metamorphic frogs exposed to paraquat.BMC biology · 2026Article
- Understanding the Pre-Clinical Stages of Parkinson's Disease: Where Are We in Clinical and Research Settings?International journal of molecular sciences · 2025Review
- Cellular mechanisms of traumatic brain injury.npj biological physics and mechanics · 2025Review
- Amyloidogenic Processing of Amyloid Precursor Protein Drives Stretch-Induced Disruption of Axonal Transport in hiPSC-Derived Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Biofidelic dynamic compression of human cortical spheroids reproduces neurotrauma phenotypes.Disease models & mechanisms · 2021Article
- Mechanical Stretching-Induced Traumatic Brain Injury Is Mediated by the Formation of GSK-3β-Tau Complex to Impair Insulin Signaling Transduction.Biomedicines · 2021Article
- Seawater Immersion Aggravates Early Mitochondrial Dysfunction and Increases Neuronal Apoptosis After Traumatic Brain Injury.Cellular and molecular neurobiology · 2020Article
- Stretch-Induced Deformation as a Model to Study Dopaminergic Dysfunction in Traumatic Brain Injury.Neurochemical research · 2019Article
- Metabolomic Responses to Manganese Dose in SH-SY5Y Human Neuroblastoma Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Cyclic stretch induced oxidative stress by mitochondrial and NADPH oxidase in retinal pigment epithelial cells.BMC ophthalmology · 2019Article
- Traumatic Brain Injury Impairs Myogenic Constriction of Cerebral Arteries: Role of Mitochondria-Derived HJournal of neurotrauma · 2018Article
- Sesamin protects SH-SY5Y cells against mechanical stretch injury and promoting cell survival.BMC neuroscience · 2017Article
- Overexpression of p58ipk protects neuroblastoma against paraquat-induced toxicity.International journal of clinical and experimental pathology · 2017Article
- Corosolic acid inhibits the proliferation of osteosarcoma cells by inducing apoptosis.Oncology letters · 2016Article
- Acetazolamide Mitigates Astrocyte Cellular Edema Following Mild Traumatic Brain Injury.Scientific reports · 2016Article
- Alzheimer's disease and chronic traumatic encephalopathy: Distinct but possibly overlapping disease entities.Brain injury · 2016Review
- Low-Dose Aronia melanocarpa Concentrate Attenuates Paraquat-Induced Neurotoxicity.Oxidative medicine and cellular longevity · 2016Article
- Emerging therapies in traumatic brain injury.Seminars in neurology · 2015Review
- Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation.Biomolecules & therapeutics · 2014Article
- Intracellular and microenvironmental regulation of mitochondrial membrane potential in cancer cells.WIREs mechanisms of diseaseReview
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Recent studies suggest that traumatic brain injury (TBI) and pesticide exposure increase the risk of Parkinson's disease (PD), but the molecular mechanisms involved remain unclear. Using an in vitro model of TBI, we evaluated the role of mitochondrial membrane potential (ΔΨm) and mitochondrial reactive oxygen species (ROS) induced by stretch on dopaminergic cell death upon paraquat exposure. Human dopaminergic neuroblastoma SH-SY5Y cells grown on silicone membrane were stretched at mild (25%) and moderate (50%) strain prior to paraquat exposure. We observed that moderate stretch (50% strain) increased the vulnerability of cells to paraquat demonstrated by the loss of plasma membrane integrity (propidium iodide-uptake) and decreased mitochondrial activity (MTT assay). Mitochondrial depolarization occurred immediately after stretch, while mitochondrial ROS increased rapidly and remained elevated for up to 4h after the stretch injury. Intracellular glutathione (GSH) stores were also transiently decreased immediately after moderate stretch. Cells treated with paraquat, or moderate stretch exhibited negligible mitochondrial depolarization at 48h post treatment, whereas in cells stretched prior to paraquat exposure, a significant mitochondrial depolarization occurred compared to samples exposed to either paraquat or stretch. Moderate stretch also increased mitochondrial ROS formation, as well as exacerbated intracellular GSH loss induced by paraquat. Overexpression of manganese superoxide dismutase (MnSOD) markedly diminished the deleterious effects of stretch in paraquat neurotoxicity. Our findings demonstrate that oxidative stress induced by mitochondrial dysfunction plays a critical role in the synergistic toxic effects of stretch (TBI) and pesticide exposure. Mitigation of oxidative stress via mitochondria-targeted antioxidants appears an attractive route for treatment of neurodegeneration mediated by TBI.
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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.