ArticleJournal of neuroscience research2008
Ethanol promotes endoplasmic reticulum stress-induced neuronal death: involvement of oxidative stress.
Article in Journal of neuroscience research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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Who cites it
39 citing papers in PubMed, 82 citations in OpenAlex.
- ER Stress Regulates HIV Tat and Alcohol-Induced NLRP6 Activation in Astrocytes.CNS neuroscience & therapeutics · 2026Article
- Neurotoxicity of Chronic Alcohol Exposure: Mechanistic Insights, Cellular Disruption, and Emerging Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Ethanol-Induced Depression: Exploring the Underlying Molecular Mechanisms.Cellular and molecular neurobiology · 2025Review
- Exploring the role of Prx II in mitigating endoplasmic reticulum stress and mitochondrial dysfunction in neurodegeneration.Cell communication and signaling : CCS · 2024Article
- Upregulation of mesencephalic astrocyte-derived neurotrophic factor (MANF) expression offers protection against alcohol neurotoxicity.Journal of neurochemistry · 2023Article
- Endoplasmic Reticulum Stress Signaling and Neuronal Cell Death.International journal of molecular sciences · 2022Review
- Potential Role of MANF, an ER Stress Responsive Neurotrophic Factor, in Protecting Against Alcohol Neurotoxicity.Molecular neurobiology · 2022Review
- Oxysterols Modulate the Acute Effects of Ethanol on HippocampalThe Journal of pharmacology and experimental therapeutics · 2021Article
- Alterations in niban gene expression as a response to stress conditions in 3T3-L1 adipocytes.Molecular biology reports · 2020Article
- Cyanidin-3-glucoside activates Nrf2-antioxidant response element and protects against glutamate-induced oxidative and endoplasmic reticulum stress in HT22 hippocampal neuronal cells.BMC complementary medicine and therapies · 2020Article
- Acetaldehyde Induces NeurotoxicityOxidative medicine and cellular longevity · 2019Article
- Binge ethanol exposure induces endoplasmic reticulum stress in the brain of adult mice.Toxicology and applied pharmacology · 2018Article
- The Neuroprotective Effects of Carvacrol on Ethanol-Induced Hippocampal Neurons Impairment via the Antioxidative and Antiapoptotic Pathways.Oxidative medicine and cellular longevity · 2017Article
- Liver-specific Gene Inactivation of the Transcription Factor ATF4 Alleviates Alcoholic Liver Steatosis in Mice.The Journal of biological chemistry · 2016Article
- Endoplasmic Reticulum Stress and Ethanol Neurotoxicity.Biomolecules · 2015Review
- Distinct inhibitory effects on mTOR signaling by ethanol and INK128 in diffuse large B-cell lymphoma.Cell communication and signaling : CCS · 2015Article
- Chronic alcohol exposure affects the cell components involved in membrane traffic in neuronal dendrites.Neurotoxicity research · 2015Article
- Hypoxic preconditioning alleviates ethanol neurotoxicity: the involvement of autophagy.Neurotoxicity research · 2013Article
- Anthocyanins protect against ethanol-induced neuronal apoptosis via GABAB1 receptors intracellular signaling in prenatal rat hippocampal neurons.Molecular neurobiology · 2013Article
- Endoplasmic reticulum stress induces fibrogenic activity in hepatic stellate cells through autophagy.Journal of hepatology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
One of the most devastating effects of ethanol exposure during development is the loss of neurons in selected brain areas. The underlying cellular/molecular mechanisms remain unclear. The endoplasmic reticulum (ER) is involved in posttranslational protein processing and transport. The accumulation of unfolded or misfolded proteins in the ER lumen triggers ER stress, which is characterized by translational attenuation, synthesis of ER chaperone proteins such as GRP78, and activation of transcription factors such as ATF4, ATF6, and CHOP. Sustained ER stress ultimately leads to cell death. ER stress response can be induced experimentally by treatment with tunicamycin and thapsigargin. Using SH-SY5Y neuroblastoma cells and primary cerebellar granule neurons as in vitro models, we demonstrated that exposure to ethanol alone had little effect on the expression of markers for ER stress; however, ethanol drastically enhanced the expression of GRP78, CHOP, ATF4, ATF6, and phosphorylated PERK and eIF2 alpha when induced by tunicamycin and thapsigargin. Consistently, ethanol promoted tunicamycin- and thapsigargin-induced cell death. Ethanol rapidly caused oxidative stress in cultured neuronal cells; antioxidants blocked ethanol's potentiation of ER stress and cell death, suggesting that the ethanol-promoted ER stress response is mediated by oxidative stress. CHOP is a proapoptotic transcription factor. We further demonstrated that CHOP played an important role in ethanol-promoted cell death. Thus, the effect of ethanol may be mediated by the interaction between oxidative stress and ER stress.
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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.