ArticleBirth defects research. Part A, Clinical and molecular teratology2011
Agrin function associated with ocular development is a target of ethanol exposure in embryonic zebrafish.
Article in Birth defects research. Part A, Clinical and molecular teratology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 48 citations in OpenAlex.
- The Role of the Hedgehog Pathway in Alcohol-Induced Birth Defects.Advances in experimental medicine and biology · 2026Review
- Bone morphogenetic protein signaling pathway- Ethanol interactions disrupt palate formation independent of gata3.Reproductive toxicology (Elmsford, N.Y.) · 2025Article
- Efcab7 deletion sensitizes mice to the teratogenic effects of gastrulation-stage alcohol exposure.Reproductive toxicology (Elmsford, N.Y.) · 2024Article
- Article
- Perturbation of 3D nuclear architecture, epigenomic dysregulation and aging, and cannabinoid synaptopathy reconfigures conceptualization of cannabinoid pathophysiology: part 1-aging and epigenomics.Frontiers in psychiatry · 2023Review
- Embryonic ethanol exposure disrupts craniofacial neuromuscular integration in zebrafish larvae.Frontiers in physiology · 2023Article
- Pharmacological activation of the Sonic hedgehog pathway with a Smoothened small molecule agonist ameliorates the severity of alcohol-induced morphological and behavioral birth defects in a zebrafish model of fetal alcohol spectrum disorder.Journal of neuroscience research · 2022Article
- Analysis of Gene-Environment Interactions Related to Developmental Disorders.Frontiers in pharmacology · 2022Review
- Zebrafish models of fetal alcohol spectrum disorders.Genesis (New York, N.Y. : 2000) · 2021Review
- Loss of tumor protein 53 protects against alcohol-induced facial malformations in mice and zebrafish.Alcoholism, clinical and experimental research · 2021Article
- Ocular measurements in fetal alcohol spectrum disorders.American journal of medical genetics. Part A · 2020Article
- Ethanol and Cannabinoids Regulate Zebrafish GABAergic Neuron Development and Behavior in a Sonic Hedgehog and Fibroblast Growth Factor-Dependent Mechanism.Alcoholism, clinical and experimental research · 2020Article
- Animal models of gene-alcohol interactions.Birth defects research · 2020Review
- Distribution and Function of Glycosaminoglycans and Proteoglycans in the Development, Homeostasis and Pathology of the Ocular Surface.Frontiers in cell and developmental biology · 2020Review
- Cannabinoids Exacerbate Alcohol Teratogenesis by a CB1-Hedgehog Interaction.Scientific reports · 2019Article
- Diving into the world of alcohol teratogenesis: a review of zebrafish models of fetal alcohol spectrum disorder.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2018Review
- Comparison of molecular marker expression in early zebrafish brain development following chronic ethanol or morpholino treatment.Experimental brain research · 2017Article
- Long-term behavioral change as a result of acute ethanol exposure in zebrafish: Evidence for a role for sonic hedgehog but not retinoic acid signaling.Neurotoxicology and teratology · 2017Article
- Prenatal ethanol exposure in mice phenocopies Cdon mutation by impeding Shh function in the etiology of optic nerve hypoplasia.Disease models & mechanisms · 2017Article
- Gene-environment interactions in development and disease.Wiley interdisciplinary reviews. Developmental biology · 2017Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAlcohol (ethanol) is a teratogen known to affect the developing eyes, face, and brain. Among the ocular defects in fetal alcohol spectrum disorder (FASD) are microphthalmia and optic nerve hypoplasia. Employing zebrafish as an FASD model provides an excellent system to analyze the molecular basis of prenatal ethanol exposure-induced defects because embryos can be exposed to ethanol at defined developmental stages and affected genetic pathways can be examined. We have previously shown that disruption of agrin function in zebrafish embryos produces microphthalmia and optic nerve hypoplasia.
methodsZebrafish embryos were exposed to varying concentrations of ethanol in the absence or presence of morpholino oligonucleotides (MOs) that disrupt agrin function. In situ hybridization was used to analyze ocular gene expression as a consequence of ethanol exposure and agrin knockdown. Morphologic analysis of zebrafish embryos was also conducted.
resultsAcute ethanol exposure induces diminished agrin gene expression in zebrafish eyes and, importantly, combined treatment with subthreshold levels of agrin MO and ethanol produces pronounced microphthalmia, markedly reduces agrin gene expression, and perturbs Pax6a and Mbx gene expression. Microphthalmia produced by combined agrin MO and ethanol treatment was rescued by sonic hedgehog (Shh) mRNA overexpression, suggesting that ethanol-mediated disruption of agrin expression results in disrupted Shh function.
conclusionsThese studies illustrate the strong potential for using zebrafish as a model to aid in defining the molecular basis for ethanol's teratogenic effects. The results of this work suggest that agrin expression and function may be a target of ethanol exposure during embryogenesis.
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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.