ArticleBirth defects research2017
Differences in neural crest sensitivity to ethanol account for the infrequency of anterior segment defects in the eye compared with craniofacial anomalies in a zebrafish model of fetal alcohol syndrome.
Article in Birth defects research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
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- Neural crest cells and fetal alcohol spectrum disorders: Mechanisms and potential targets for prevention.Pharmacological research · 2023Review
- [Notch signaling pathway inhibitor DAPT improves alcohol-induced neuronal differentiation impairment in zebrafish].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Embryonic ethanol exposure disrupts craniofacial neuromuscular integration in zebrafish larvae.Frontiers in physiology · 2023Article
- Zebrafish Model of Stickler Syndrome Suggests a Role for Col2a1a in the Neural Crest during Early Eye Development.Journal of developmental biology · 2022Article
- Zebrafish models of alx-linked frontonasal dysplasia reveal a role for Alx1 and Alx3 in the anterior segment and vasculature of the developing eye.Biology open · 2022Article
- Loss of tumor protein 53 protects against alcohol-induced facial malformations in mice and zebrafish.Alcoholism, clinical and experimental research · 2021Article
- Vitamin E: necessary nutrient for neural development and cognitive function.The Proceedings of the Nutrition Society · 2021Article
- Genetics Underlying the Interactions between Neural Crest Cells and Eye Development.Journal of developmental biology · 2020Review
- Vitamin E is necessary for zebrafish nervous system development.Scientific reports · 2020Article
- The Ocular Neural Crest: Specification, Migration, and Then What?Frontiers in cell and developmental biology · 2020Review
- Zebrafish Models of Craniofacial Malformations: Interactions of Environmental Factors.Frontiers in cell and developmental biology · 2020Review
- Clinical presentation, diagnosis, and management of fetal alcohol spectrum disorder.The Lancet. Neurology · 2019Review
- Review of evidence for environmental causes of uveal coloboma.Survey of ophthalmologyReview
- Extrahepatic Manifestations in Alcoholic Liver Disease.Journal of clinical and experimental hepatologyReview
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEthanol (ETOH) exposure during pregnancy is associated with craniofacial and neurologic abnormalities, but infrequently disrupts the anterior segment of the eye. In these studies, we used zebrafish to investigate differences in the teratogenic effect of ETOH on craniofacial, periocular, and ocular neural crest.
methodsZebrafish eye and neural crest development was analyzed by means of live imaging, TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assay, immunostaining, detection of reactive oxygen species, and in situ hybridization.
resultsOur studies demonstrated that foxd3-positive neural crest cells in the periocular mesenchyme and developing eye were less sensitive to ETOH than sox10-positive craniofacial neural crest cells that form the pharyngeal arches and jaw. ETOH increased apoptosis in the retina, but did not affect survival of periocular and ocular neural crest cells. ETOH also did not increase reactive oxygen species within the eye. In contrast, ETOH increased ventral neural crest apoptosis and reactive oxygen species production in the facial mesenchyme. In the eye and craniofacial region, sod2 showed high levels of expression in the anterior segment and in the setting of Sod2 knockdown, low levels of ETOH decreased migration of foxd3-positive neural crest cells into the developing eye. However, ETOH had minimal effect on the periocular and ocular expression of transcription factors (pitx2 and foxc1) that regulate anterior segment development.
conclusionNeural crest cells contributing to the anterior segment of the eye exhibit increased ability to withstand ETOH-induced oxidative stress and apoptosis. These studies explain the rarity of anterior segment dysgenesis despite the frequent craniofacial abnormalities in fetal alcohol syndrome. Birth Defects Research 109:1212-1227, 2017. © 2017 Wiley Periodicals, Inc.
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