ArticleAlcoholism, clinical and experimental research2011
Ethanol-induced microphthalmia is not mediated by changes in retinoic acid or sonic hedgehog signaling during retinal neurogenesis.
Article in Alcoholism, clinical and experimental research, 2011. 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, 39 citations in OpenAlex.
- The Role of the Hedgehog Pathway in Alcohol-Induced Birth Defects.Advances in experimental medicine and biology · 2026Review
- 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
- Zebrafish models of fetal alcohol spectrum disorders.Genesis (New York, N.Y. : 2000) · 2021Review
- Selective Requirements for Vascular Endothelial Cells and Circulating Factors in the Regulation of Retinal Neurogenesis.Frontiers in cell and developmental biology · 2021Article
- Animal models of gene-alcohol interactions.Birth defects research · 2020Review
- 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
- Article
- Gene-environment interactions in development and disease.Wiley interdisciplinary reviews. Developmental biology · 2017Review
- Fishing for Fetal Alcohol Spectrum Disorders: Zebrafish as a Model for Ethanol Teratogenesis.Zebrafish · 2016Review
- The Genetics of Fetal Alcohol Spectrum Disorders.Alcoholism, clinical and experimental research · 2016Review
- Analysis of crosstalk between retinoic acid and sonic hedgehog pathways following ethanol exposure in embryonic zebrafish.Birth defects research. Part A, Clinical and molecular teratology · 2015Article
- Abnormal retinal development in Cloche mutant zebrafish.Developmental dynamics : an official publication of the American Association of Anatomists · 2015Article
- Retinoic Acid Signaling Regulates Differential Expression of the Tandemly-Duplicated Long Wavelength-Sensitive Cone Opsin Genes in Zebrafish.PLoS genetics · 2015Article
- Zebrafish retinal defects induced by ethanol exposure are rescued by retinoic acid and folic acid supplement.Alcohol (Fayetteville, N.Y.) · 2015Article
- An evolutionarily conserved mechanism of calcium-dependent neurotoxicity in a zebrafish model of fetal alcohol spectrum disorders.Alcoholism, clinical and experimental research · 2014Article
- Eye-specific gene expression following embryonic ethanol exposure in zebrafish: roles for heat shock factor 1.Reproductive toxicology (Elmsford, N.Y.) · 2014Article
- Complex cardiac defects after ethanol exposure during discrete cardiogenic events in zebrafish: prevention with folic acid.Developmental dynamics : an official publication of the American Association of Anatomists · 2013Article
- Fetal Alcohol Spectrum Disorder (FASD) Associated Neural Defects: Complex Mechanisms and Potential Therapeutic Targets.Brain sciences · 2013Article
- Ethanol affects the development of sensory hair cells in larval zebrafish (Danio rerio).PloS one · 2013Article
- Forebrain and hindbrain development in zebrafish is sensitive to ethanol exposure involving agrin, Fgf, and sonic hedgehog function.Birth defects research. Part A, Clinical and molecular teratology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMicrophthalmia (reduced eye size), generally accompanied by vision defects, is a hallmark of fetal alcohol spectrum disorder (FASD) in humans. In zebrafish, embryonic ethanol exposure over the time of retinal neurogenesis also results in microphthalmia. This microphthalmia is in part the consequence of reduced retinal cell differentiation, including photoreceptors. Here we pursue 2 signaling pathways implicated in other aspects of FASD pathogenesis: retinoic acid (RA) and Sonic hedgehog (Shh).
methodsWe evaluated markers for RA and Shh signaling within the eyes of embryos treated with ethanol during the period of retinal neurogenesis. We also performed rescue experiments using administration of exogenous RA and microinjection of cholesterol, which augments Shh signaling.
resultsUsing sequential or co-treatments, RA did not rescue ethanol-induced microphthalmia at any concentration tested. In addition, RA itself caused microphthalmia, although the underlying mechanisms were distinct from those of ethanol. Interestingly, RA treatment appeared to recover photoreceptor differentiation in a concentration-dependent manner. This may be an independent effect of exogenous RA, as ethanol treatment alone did not alter RA signaling in the eye. Cholesterol injection also did not rescue ethanol-induced microphthalmia at any concentration tested, and ethanol treatments did not alter expression of shh, or of ptc-2, which is normally regulated by Shh signaling.
conclusionsTogether these findings indicate that, during the time of retinal neurogenesis, effects of ethanol on eye development are likely independent of the RA and Shh signaling pathways. These studies suggest that FASD intervention strategies based upon augmentation of RA or Shh signaling may not prevent ethanol-induced microphthalmia.
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