ArticleMetabolic brain disease2013
Expression of autophagy and UPR genes in the developing brain during ethanol-sensitive and resistant periods.
Article in Metabolic brain disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Impact of Prenatal Alcohol Exposure on the Cerebral Circulation: Potential Implications for Stroke.Advances in experimental medicine and biology · 2026Review
- Environmental adversity, endoplasmic reticulum stress, and neurogenesis.Neurotoxicology · 2025Review
- Roles of Oxidative Stress and Autophagy in Alcohol-Mediated Brain Damage.Antioxidants (Basel, Switzerland) · 2025Review
- Sex-specific effects of alcohol on neurobehavioral performance and endoplasmic reticulum stress: an analysis using neuron-specific MANF deficient mice.Frontiers in pharmacology · 2024Article
- Effects of Genetics and Sex on Acute Gene Expression Changes in the Hippocampus Following Neonatal Ethanol Exposure in BXD Recombinant Inbred Mouse Strains.Brain sciences · 2022Article
- Potential Role of MANF, an ER Stress Responsive Neurotrophic Factor, in Protecting Against Alcohol Neurotoxicity.Molecular neurobiology · 2022Review
- Prenatal exposure to alcohol: mechanisms of cerebral vascular damage and lifelong consequences.Advances in drug and alcohol research · 2022Review
- ERAD components Derlin-1 and Derlin-2 are essential for postnatal brain development and motor function.iScience · 2021Article
- Minocycline attenuates ethanol-induced cell death and microglial activation in the developing spinal cord.Alcohol (Fayetteville, N.Y.) · 2019Article
- 4-Phenylbutyric Acid Protects Against Ethanol-Induced Damage in the Developing Mouse Brain.Alcoholism, clinical and experimental research · 2019Article
- Role of MCP-1 and CCR2 in ethanol-induced neuroinflammation and neurodegeneration in the developing brain.Journal of neuroinflammation · 2018Article
- Zika Virus as an Emerging Neuropathogen: Mechanisms of Neurovirulence and Neuro-Immune Interactions.Molecular neurobiology · 2018Review
- Minocycline protects developing brain against ethanol-induced damage.Neuropharmacology · 2018Article
- Journey to the Center of the Fetal Brain: Environmental Exposures and Autophagy.Frontiers in cellular neuroscience · 2018Review
- Prenatal alcohol exposure impairs autophagy in neonatal brain cortical microvessels.Cell death & disease · 2017Article
- The Role of CYP2E1 in the Drug Metabolism or Bioactivation in the Brain.Oxidative medicine and cellular longevity · 2017Review
- Ethanol-mediated activation of the NLRP3 inflammasome in iPS cells and iPS cells-derived neural progenitor cells.Molecular brain · 2016Article
- Endoplasmic Reticulum Stress and Ethanol Neurotoxicity.Biomolecules · 2015Review
- Ethanol Attenuates Histiotrophic Nutrition Pathways and Alters the Intracellular Redox Environment and Thiol Proteome during Rat Organogenesis.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- Exposure of neonatal rats to alcohol has differential effects on neuroinflammation and neuronal survival in the cerebellum and hippocampus.Journal of neuroinflammation · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Fetal alcohol spectrum disorders (FASD) results from ethanol exposure to the developing fetus and is the leading cause of mental retardation. FASD is associated with a broad range of neurobehavioral deficits which may be mediated by ethanol-induced neurodegeneration in the developing brain. An immature brain is more susceptible to ethanol neurotoxicity. We hypothesize that the enhanced sensitivity of the immature brain to ethanol is due to a limited capacity to alleviate cellular stress. Using a third trimester equivalent mouse model of ethanol exposure, we demonstrated that subcutaneous injection of ethanol induced a wide-spread neuroapoptosis in postnatal day 4 (PD4) C57BL/6 mice, but had little effect on the brain of PD12 mice. We analyzed the expression profile of genes regulating apoptosis, and the pathways of ER stress response (also known as unfolded protein response, UPR) and autophagy during these ethanol-sensitive and resistant periods (PD4 versus PD12) using PCR microarray. The expression of pro-apoptotic genes, such as caspase-3, was much higher on PD4 than PD12; in contrast, the expression of genes that regulate UPR and autophagy, such as atf6, atg4, atg9, atg10, beclin1, bnip3, cebpb, ctsb, ctsd, ctss, grp78, ire1α, lamp, lc3 perk, pik3c3, and sqstm1 was significantly higher on PD12 than PD4. These results suggest that the vulnerability of the immature brain to ethanol could result from high expression of pro-apoptotic proteins and a deficiency in the stress responsive system, such as UPR and autophagy.
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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.