June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Ocular neural crest cells are less sensitive to ethanol than craniofacial neural crest in a zebrafish model of fetal alcohol syndrome
Author Affiliations & Notes
  • Jessica Eason
    Department of Ophthalmology and Visual S, Univ of Michigan Kellogg Eye Center, Ann Arbor, Michigan, United States
  • Antionette L. Williams
    Department of Ophthalmology and Visual S, Univ of Michigan Kellogg Eye Center, Ann Arbor, Michigan, United States
  • Bahaar Chawla
    Department of Ophthalmology and Visual S, Univ of Michigan Kellogg Eye Center, Ann Arbor, Michigan, United States
  • Christian Apsey
    Department of Ophthalmology and Visual S, Univ of Michigan Kellogg Eye Center, Ann Arbor, Michigan, United States
  • Brenda L Bohnsack
    Department of Ophthalmology and Visual S, Univ of Michigan Kellogg Eye Center, Ann Arbor, Michigan, United States
  • Footnotes
    Commercial Relationships   Jessica Eason, None; Antionette L. Williams, None; Bahaar Chawla, None; Christian Apsey, None; Brenda Bohnsack, None
  • Footnotes
    Support  KO8EY022912-01
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 3004. doi:
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    • Get Citation

      Jessica Eason, Antionette L. Williams, Bahaar Chawla, Christian Apsey, Brenda L Bohnsack; Ocular neural crest cells are less sensitive to ethanol than craniofacial neural crest in a zebrafish model of fetal alcohol syndrome. Invest. Ophthalmol. Vis. Sci. 2017;58(8):3004.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Ethanol (ETOH) exposure during pregnancy is associated with craniofacial and neurologic abnormalities, but rarely causes anterior segment dysgenesis. In these studies, we used zebrafish to investigate the molecular differences in the teratogenic effect of ETOH on craniofacial and ocular neural crest.

Methods : Zebrafish eye and neural crest development were analyzed via live imaging, TUNEL assay, immunostaining, detection of reactive oxygen species, and in situ hybridization.

Results : Treatment with increasing concentrations of ETOH from 24-48 hours post fertilization (hpf) targeted craniofacial and ocular neural crest migration, survival and differentiation. Exposure to 1% ETOH increased reactive oxygen species in the periocular and facial neural crest (B, arrows) resulting in increased apoptosis (E, arrowheads) compared to untreated controls (A, D). In contrast, 1% ETOH did not induce oxidative stress nor affect survival of ocular neural crest cells. As a result, embryos treated with 1% ETOH showed delayed pharyngeal arch and jaw formation (K), but normal ocular neural crest migration (H, arrow) and iris stroma formation (N, arrowheads) compared to untreated controls (G, J, M). Treatment with 3% ETOH decreased craniofacial and ocular neural crest migration (I, arrow) and survival (F, arrowhead) resulting in severe jaw, pharyngeal arch (L), and anterior segment (O) abnormalities. 3% ETOH increased oxidative reactive species in the periocular and facial mesenchyme and in the retina (C), but not in the ocular neural crest. Although low concentrations of ETOH did not alter anterior segment development, 1% or 3% ETOH inhibited expression of pitx2a, foxc1a, foxc1b, and cyp1b1, suggesting that these genes direct ocular neural crest development outside the timeframe of ETOH exposure.

Conclusions : Ocular neural crest cells are less sensitive to the teratogenic effects of ETOH. This difference may be due to a better ability to withstand ETOH-induced oxidative stress and suggests that ocular neural crest cells are distinct from craniofacial neural crest cells. These studies help to explain the rarity of anterior segment dysgenesis despite the frequent craniofacial abnormalities in the setting of fetal alcohol syndrome.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

 

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