ArticleInternational journal of molecular sciences2019
Alpha-Tocotrienol Prevents Oxidative Stress-Mediated Post-Translational Cleavage of Bcl-xL in Primary Hippocampal Neurons.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Bedaquiline inhibits the ATP synthase leak channel and prevents glutamate-induced neuronal death.Biophysical reports · 2026Article
- Mitochondrial Metabolic Reprogramming of Cortical Neurons by Prenatal Exposure to Corticosterone: A Shift from ATP Synthesis to Membrane Potential Maintenance.Experimental neurobiology · 2026Article
- Bedaquiline inhibits the ATP synthase leak channel and prevents glutamate-induced neuronal death.bioRxiv : the preprint server for biology · 2026Article
- Fluid shear stress enhances proliferation of breast cancer cells via downregulation of the c-subunit of the FBiochemical and biophysical research communications · 2022Article
- Revisiting the therapeutic potential of tocotrienol.BioFactors (Oxford, England) · 2022Review
- Alpha-tocotrienol enhances arborization of primary hippocampal neurons via upregulation of Bcl-xL.Nutrition research (New York, N.Y.) · 2022Article
- CationicMolecules (Basel, Switzerland) · 2022Article
- Neuroprotective effects of ATPase inhibitory factor 1 preventing mitochondrial dysfunction in Parkinson's disease.Scientific reports · 2022Article
- Bcl-xL Is Required by Primary Hippocampal Neurons during Development to Support Local Energy Metabolism at Neurites.Biology · 2021Article
- Article
- An Interactive Review on the Role of Tocotrienols in the Neurodegenerative Disorders.Frontiers in nutrition · 2021Review
- Oxidative stress battles neuronal Bcl-xL in a fight to the death.Neural regeneration research · 2021Article
- Anti-Apoptotic Effects of Carotenoids in Neurodegeneration.Molecules (Basel, Switzerland) · 2020Review
- Cellular Mechanisms of Circulating Tumor Cells During Breast Cancer Metastasis.International journal of molecular sciences · 2020Review
- Dietary Antioxidants and Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
B-cell lymphoma-extra large (Bcl-xL) is an anti-apoptotic member of the Bcl2 family of proteins, which supports neurite outgrowth and neurotransmission by improving mitochondrial function. During excitotoxic stimulation, however, Bcl-xL undergoes post-translational cleavage to ∆N-Bcl-xL, and accumulation of ∆N-Bcl-xL causes mitochondrial dysfunction and neuronal death. In this study, we hypothesized that the generation of reactive oxygen species (ROS) during excitotoxicity leads to formation of ∆N-Bcl-xL. We further proposed that the application of an antioxidant with neuroprotective properties such as α-tocotrienol (TCT) will prevent ∆N-Bcl-xL-induced mitochondrial dysfunction via its antioxidant properties. Primary hippocampal neurons were treated with α-TCT, glutamate, or a combination of both. Glutamate challenge significantly increased cytosolic and mitochondrial ROS and ∆N-Bcl-xL levels. ∆N-Bcl-xL accumulation was accompanied by intracellular ATP depletion, loss of mitochondrial membrane potential, and cell death. α-TCT prevented loss of mitochondrial membrane potential in hippocampal neurons overexpressing ∆N-Bcl-xL, suggesting that ∆N-Bcl-xL caused the loss of mitochondrial function under excitotoxic conditions. Our data suggest that production of ROS is an important cause of ∆N-Bcl-xL formation and that preventing ROS production may be an effective strategy to prevent ∆N-Bcl-xL-mediated mitochondrial dysfunction and thus promote neuronal survival.
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Registered trials
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