ArticleCells2019
Increasing the TRPM2 Channel Expression in Human Neuroblastoma SH-SY5Y Cells Augments the Susceptibility to ROS-Induced Cell Death.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- Brain-derived neurotrophic factor via TRPM2 inhibition reduces amyloid-beta-mediated increases of apoptosis and mitochondrial oxidative neurotoxicity in neuronal cells.Metabolic brain disease · 2026Article
- Glutathione Decreases Parkinsonism-Induced Ferroptosis and Oxidative Stress Through the Inhibition of the TRPM2 Channel in Neuronal Cells.Pharmacology research & perspectives · 2025Article
- Targeting Transient Receptor Potential Melastatin-2 (TRPM2) Enhances Therapeutic Efficacy of Third Generation EGFR Inhibitors against EGFR Mutant Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Molecular mechanisms of cell death by parthanatos: More questions than answers.Genetics and molecular biology · 2024Article
- Neural regeneration research model to be explored: SH-SY5Y human neuroblastoma cells.Neural regeneration research · 2023Article
- Neuroprotective Effect of 2-Aminoethoxydiphenyl Borate (2-APB) in Amyloid β-Induced Memory Dysfunction: A Mechanistic Study.Cellular and molecular neurobiology · 2022Article
- Pharmacological Modulation of TRPM2 Channels via PARP Pathway Leads to Neuroprotection in MPTP-induced Parkinson's Disease in Sprague Dawley Rats.Molecular neurobiology · 2022Article
- Inhibition of TRPM2 by AG490 Is Neuroprotective in a Parkinson's Disease Animal Model.Molecular neurobiology · 2022Article
- Two Benzene Rings with a Boron Atom Comprise the Core Structure of 2-APB Responsible for the Anti-Oxidative and Protective Effect on the Ischemia/Reperfusion-Induced Rat Heart Injury.Antioxidants (Basel, Switzerland) · 2021Article
- Cannabidiol modulation of oxidative stress and signalling.Neuronal signaling · 2021Review
- Curcumin Attenuates Hypoxia-Induced Oxidative Neurotoxicity, Apoptosis, Calcium, and Zinc Ion Influxes in a Neuronal Cell Line: Involvement of TRPM2 Channel.Neurotoxicity research · 2021Article
- Nucleoredoxin Knockdown in SH-SY5Y Cells Promotes Cell Renewal.Antioxidants (Basel, Switzerland) · 2021Article
- Roles of NADMolecules (Basel, Switzerland) · 2020Review
- TRPM2 channel-mediated cell death: An important mechanism linking oxidative stress-inducing pathological factors to associated pathological conditions.Redox biology · 2020Review
- Glutathione Depletion and Parkinsonian Neurotoxin MPPMolecular neurobiology · 2020Article
- Article
- Transient Receptor Potential Channels as an Emerging Target for the Treatment of Parkinson's Disease: An Insight Into Role of Pharmacological Interventions.Frontiers in cell and developmental biology · 2020Review
- Curcumin enhances cisplatin-induced human laryngeal squamous cancer cell death through activation of TRPM2 channel and mitochondrial oxidative stress.Scientific reports · 2019Article
- A Role for HAntioxidants (Basel, Switzerland) · 2019Article
- Albumin evokes CaScientific reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human neuroblastoma SH-SY5Y cells are a widely-used human neuronal cell model in the study of neurodegeneration. A recent study shows that, 1-methyl-4-phenylpyridine ion (MPP), which selectively causes dopaminergic neuronal death leading to Parkinson's disease-like symptoms, can reduce SH-SY5Y cell viability by inducing H₂O₂ generation and subsequent TRPM2 channel activation. MPP-induced cell death is enhanced by increasing the TRPM2 expression. By contrast, increasing the TRPM2 expression has also been reported to support SH-SY5Y cell survival after exposure to H₂O₂, leading to the suggestion of a protective role for the TRPM2 channel. To clarify the role of reactive oxygen species (ROS)-induced TRPM2 channel activation in SH-SY5Y cells, we generated a stable SH-SY5Y cell line overexpressing the human TRPM2 channel and examined cell death and cell viability after exposure to H₂O₂ in the wild-type and TRPM2-overexpressing SH-SY5Y cells. Exposure to H₂O₂ resulted in concentration-dependent cell death and reduction in cell viability in both cell types. TRPM2 overexpression remarkably augmented H₂O₂-induced cell death and reduction in cell viability. Furthermore, H₂O₂-induced cell death in both the wild-type and TRPM2-overexpressing cells was prevented by 2-APB, a TRPM2 inhibitor, and also by PJ34 and DPQ, poly(ADP-ribose) polymerase (PARP) inhibitors. Collectively, our results show that increasing the TRPM2 expression renders SH-SY5Y cells to be more susceptible to ROS-induced cell death and reinforce the notion that the TRPM2 channel plays a critical role in conferring ROS-induced cell death. It is anticipated that SH-SY5Y cells can be useful for better understanding the molecular and signaling mechanisms for ROS-induced TRPM2-mediated neurodegeneration in the pathogenesis of neurodegenerative diseases.
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