ArticleAlcoholism, clinical and experimental research2013
Suppression and epigenetic regulation of MiR-9 contributes to ethanol teratology: evidence from zebrafish and murine fetal neural stem cell models.
Article in Alcoholism, clinical and experimental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- 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
- Infant circulating MicroRNAs as biomarkers of effect in fetal alcohol spectrum disorders.Scientific reports · 2021Trial
- Zebrafish mecp2 null-mutation increases anxiety and cortisol levels but no change in adult social preference and larval chemically-induced hyperlocomotion.BMC neuroscience · 2025Article
- Recent Advances in the Role of Non-coding RNAs in Fetal Alcohol Spectrum Disorders.Advances in experimental medicine and biology · 2025Review
- Noncoding RNA and Alcohol Use Disorder: A Scoping Review of Current Research and Knowledge Gaps.Alcohol research : current reviews · 2025Article
- Nutrient Supplementation during the Prenatal Period in Substance-Using Mothers: A Narrative Review of the Effects on Offspring Development.Nutrients · 2023Review
- 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
- miR-9 utilizes precursor pathways in adaptation to alcohol in mouse striatal neurons.Advances in drug and alcohol research · 2023Article
- Prenatal alcohol exposure results in brain region- and sex-specific changes inFrontiers in neuroscience · 2023Article
- Vascular Contributions to the Neurobiological Effects of Prenatal Alcohol Exposure.Advances in drug and alcohol research · 2023Article
- Article
- Investigating the effects of chronic perinatal alcohol and combined nicotine and alcohol exposure on dopaminergic and non-dopaminergic neurons in the VTA.Scientific reports · 2021Article
- Extracellular Vesicles in CNS Developmental Disorders.International journal of molecular sciences · 2020Review
- Prenatal Alcohol Exposure Results in Sex-Specific Alterations in Circular RNA Expression in the Developing Mouse Brain.Frontiers in neuroscience · 2020Article
- Article
- Zebrafish as an integrative vertebrate model to identify miRNA mechanisms regulating toxicity.Toxicology reports · 2020Review
- Serum miRNAs are differentially altered by ethanol and caffeine consumption in rats.Toxicology research · 2019Article
- Ethanol Exposure Increases miR-140 in Extracellular Vesicles: Implications for Fetal Neural Stem Cell Proliferation and Maturation.Alcoholism, clinical and experimental research · 2019Article
- Epigenetic effects of environmental chemicals: insights from zebrafish.Current opinion in toxicology · 2017Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundFetal alcohol exposure produces multiorgan defects, making it difficult to identify underlying etiological mechanisms. However, recent evidence for ethanol (EtOH) sensitivity of the miRNA miR-9 suggests one mechanism, whereby EtOH broadly influences development. We hypothesized that loss of miR-9 function recapitulates aspects of EtOH teratology.
methodsZebrafish embryos were exposed to EtOH during gastrulation, or injected with anti-miR-9 or nonsense control morpholinos during the 2-cell stage of development and collected between 24 and 72 hours postfertilization (hpf). We also assessed the expression of developmentally important, and known miR-9 targets, FGFR-1, FOXP2, and the nontargeted transcript, MECP2. Methylation at CpG islands of mammalian miR-9 genes was assessed in fetal murine neural stem cells (mNSCs) by methylation-specific PCR, and miRNA processing assessed by qRT-PCR for pre-miR-9 transcripts.
resultsEtOH treatment and miR-9 knockdown resulted in similar cranial defects including microcephaly. Additionally, EtOH transiently suppressed miR-9, as well as FGFR-1 and FOXP2, and alterations in miR-9 expression were correlated with severity of EtOH-induced teratology. In mNSCs, EtOH increased CpG dinucleotide methylation at the miR-9-2 locus and accumulation of pre-miR-9-3.
conclusionsEtOH exerts regulatory control at multiple levels of miR-9 biogenesis. Moreover, early embryonic loss of miR-9 function recapitulated the severe range of teratology associated with developmental EtOH exposure. EtOH also disrupts the relationship between miR-9 and target gene expression, suggesting a nuanced relationship between EtOH and miRNA regulatory networks in the developing embryo. The implications of these data for the expression and function of mature miR-9 warrant further investigation.
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