ArticleAlcoholism, clinical and experimental research2012
Opposing actions of ethanol and nicotine on microRNAs are mediated by nicotinic acetylcholine receptors in fetal cerebral cortical-derived neural progenitor cells.
Article in Alcoholism, clinical and experimental research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 3 of them syntheses that pooled it.
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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
49 citing papers in PubMed, 3 syntheses or guidelines pooled it, 94 citations in OpenAlex.
- miRNAs and Substances Abuse: Clinical and Forensic Pathological Implications: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- The importance of non-coding RNAs in environmental stress-related developmental brain disorders: A systematic review of evidence associated with exposure to alcohol, anesthetic drugs, nicotine, and viral infections.Neuroscience and biobehavioral reviews · 2021Pooled it
- Role of microRNAs in the pathophysiology of addiction.Wiley interdisciplinary reviews. RNA · 2021Pooled it
- Infant circulating MicroRNAs as biomarkers of effect in fetal alcohol spectrum disorders.Scientific reports · 2021Trial
- Circular RNA RORβ regulates TGFβR1 in alcohol-induced fibroblast-to-myofibroblast differentiation.Scientific reports · 2025Article
- Noncoding RNA and Alcohol Use Disorder: A Scoping Review of Current Research and Knowledge Gaps.Alcohol research : current reviews · 2025Article
- Fetal Brain-Derived Exosomal miRNAs from Maternal Blood: Potential Diagnostic Biomarkers for Fetal Alcohol Spectrum Disorders (FASDs).International journal of molecular sciences · 2024Article
- Assessing the effects of prenatal poly-drug exposure on fetal brain vasculature using optical coherence angiography.Journal of biomedical optics · 2023Article
- Sex differences in the transcriptome of extracellular vesicles secreted by fetal neural stem cells and effects of chronic alcohol exposure.Biology of sex differences · 2023Article
- The role of microRNAs in nicotine signaling.EXCLI journal · 2023Review
- Article
- Epigenetics and Neuroinflammation Associated With Neurodevelopmental Disorders: A Microglial Perspective.Frontiers in cell and developmental biology · 2022Review
- Review
- Altering Cell-Cell Interaction in Prenatal Alcohol Exposure Models: Insight on Cell-Adhesion Molecules During Brain Development.Frontiers in molecular neuroscience · 2021Review
- Intersection of Epigenetic and Immune Alterations: Implications for Fetal Alcohol Spectrum Disorder and Mental Health.Frontiers in neuroscience · 2021Review
- MicroRNAs Dysregulation and Mitochondrial Dysfunction in Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Sex Differences in the Expression of the α5 Subunit of the GABAAlcoholism, clinical and experimental research · 2020Article
- Murine Models for the Study of Fetal Alcohol Spectrum Disorders: An Overview.Frontiers in pediatrics · 2020Review
- Ethanol Exposure Increases miR-140 in Extracellular Vesicles: Implications for Fetal Neural Stem Cell Proliferation and Maturation.Alcoholism, clinical and experimental research · 2019Article
- Effects of ethanol and varenicline on female Sprague-Dawley rats in a third trimester model of fetal alcohol syndrome.Alcohol (Fayetteville, N.Y.) · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEthanol (EtOH) and nicotine are often co-abused. However, their combined effects on fetal neural development, particularly on fetal neural stem cells (NSCs), which generate most neurons of the adult brain during the second trimester of pregnancy, are poorly understood. We previously showed that EtOH influenced NSC maturation in part, by suppressing the expression of specific microRNAs (miRNAs). Here, we tested in fetal NSCs the extent to which EtOH and nicotine coregulated known EtOH-sensitive (miR-9, miR-21, miR-153, and miR-335), a nicotine-sensitive miRNA (miR-140-3p), and mRNAs for nicotinic acetylcholine receptor (nAChR) subunits. Additionally, we tested the extent to which these effects were nAChR dependent.
methodsGestational day 12.5 mouse fetal murine cerebral cortical-derived neurosphere cultures were exposed to EtOH, nicotine, and mecamylamine, a noncompetitive nAChR antagonist, individually or in combination, for short (24 hour) and long (5 day) periods, to mimic exposure during the in vivo period of neurogenesis. Levels of miRNAs, miRNA-regulated transcripts, and nAChR subunit mRNAs were assessed by quantitative reverse transcription polymerase chain reaction.
resultsEtOH suppressed the expression of known EtOH-sensitive miRNAs and miR-140-3p, while nicotine at concentrations attained by cigarette smokers induced a dose-related increase in these miRNAs. Nicotine's effect was blocked by EtOH and by mecamylamine. Finally, EtOH decreased the expression of nAChR subunit mRNAs and, like mecamylamine, prevented the nicotine-associated increase in α4 and β2 nAChR transcripts.
conclusionsEtOH and nicotine exert mutually antagonistic, nAChR-mediated effects on teratogen-sensitive miRNAs in fetal NSCs. These data suggest that concurrent exposure to EtOH and nicotine disrupts miRNA regulatory networks that are important for NSC maturation.
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