ArticleCell death & disease2010
Prenatal alcohol exposure triggers ceramide-induced apoptosis in neural crest-derived tissues concurrent with defective cranial development.
Article in Cell death & disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 52 citations in OpenAlex.
- Neural crest cells and fetal alcohol spectrum disorders: Mechanisms and potential targets for prevention.Pharmacological research · 2023Review
- The ameliorative effects of choline on ethanol-induced cell death in the neural tube of susceptible BXD strains of mice.Frontiers in neuroscience · 2023Article
- Citicoline: pharmacological and clinical review, 2022 update.Revista de neurologia · 2022Review
- Effect of Embryonic Alcohol Exposure on Craniofacial and Skin Melanocyte Development: Insights from Zebrafish (Toxics · 2022Article
- Concomitant genetic defects potentiate the adverse impact of prenatal alcohol exposure on cardiac outflow tract maturation.Birth defects research · 2022Article
- Transcriptome-Wide Regulation of Key Developmental Pathways in the Mouse Neural Tube by Prenatal Alcohol Exposure.Alcoholism, clinical and experimental research · 2020Article
- A global lipid map defines a network essential for Zika virus replication.Nature communications · 2020Article
- Sphingolipids in neurodegeneration (with focus on ceramide and S1P).Advances in biological regulation · 2018Review
- Fetal alcohol spectrum disorders: Zebrafish in the analysis of the milder and more prevalent form of the disease.Behavioural brain research · 2018Review
- The role of sphingolipids in psychoactive drug use and addiction.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Supplementation with the Methyl Donor Betaine Prevents Congenital Defects Induced by Prenatal Alcohol Exposure.Alcoholism, clinical and experimental research · 2017Article
- Cardiac neural crest ablation results in early endocardial cushion and hemodynamic flow abnormalities.American journal of physiology. Heart and circulatory physiology · 2016Article
- Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage.Oxidative medicine and cellular longevity · 2016Review
- 5-Mehtyltetrahydrofolate rescues alcohol-induced neural crest cell migration abnormalities.Molecular brain · 2014Article
- Ethanol exposure alters early cardiac function in the looping heart: a mechanism for congenital heart defects?American journal of physiology. Heart and circulatory physiology · 2014Article
- Fetal Alcohol Spectrum Disorder (FASD) Associated Neural Defects: Complex Mechanisms and Potential Therapeutic Targets.Brain sciences · 2013Article
- Involvement of sphingolipids in ethanol neurotoxicity in the developing brain.Brain sciences · 2013Article
- Commonality in Down and fetal alcohol syndromes.Birth defects research. Part A, Clinical and molecular teratology · 2013Article
- It's a lipid's world: bioactive lipid metabolism and signaling in neural stem cell differentiation.Neurochemical research · 2012Review
- Introduction to the fractality principle of consciousness and the sentyon postulate.Cognitive computation · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fetal alcohol syndrome (FAS) is caused by maternal alcohol consumption during pregnancy. The reason why specific embryonic tissues are sensitive toward ethanol is not understood. We found that in neural crest-derived cell (NCC) cultures from the first branchial arch of E10 mouse embryos, incubation with ethanol increases the number of apoptotic cells by fivefold. Apoptotic cells stain intensely for ceramide, suggesting that ceramide-induced apoptosis mediates ethanol damage to NCCs. Apoptosis is reduced by incubation with CDP-choline (citicoline), a precursor for the conversion of ceramide to sphingomyelin. Consistent with NCC cultures, ethanol intubation of pregnant mice results in ceramide elevation and increased apoptosis of NCCs in vivo. Ethanol also increases the protein level of prostate apoptosis response 4 (PAR-4), a sensitizer to ceramide-induced apoptosis. Prenatal ethanol exposure is concurrent with malformation of parietal bones in 20% of embryos at day E18. Meninges, a tissue complex derived from NCCs, is disrupted and generates reduced levels of TGF-β1, a growth factor critical for bone and brain development. Ethanol-induced apoptosis of NCCs leading to defects in the meninges may explain the simultaneous presence of cranial bone malformation and cognitive retardation in FAS. In addition, our data suggest that treatment with CDP-choline may alleviate the tissue damage caused by alcohol.
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