The different effects on cranial and trunk neural crest cell behaviour following exposure to a low concentration of alcohol in vitro

Czarnobaj, Joanna; Bagnall, K. M.; Bamforth, John Steven; Milos, Nadine C.

doi:10.1016/j.archoralbio.2014.02.005

Cited by 18 publications

(18 citation statements)

References 40 publications

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“…When cultured in ethanol's presence (10.9 or 150 mM), fewer neural crest cells emerge from cranial-derived explants (Czarnobaj et al, 2014). The cranial neural crest cells (CNCs) travel significantly shorter distances (50% of control values) and their migration is less directional, again with more retrograde movements (Rovasio and Battiato, 2002;Czarnobaj et al, 2014). At low ethanol (10.9 mM) only the migration of cranial populations was impaired (Czarnobaj et al, 2014), and it took substantially higher ethanol levels (150 mM) to impair trunk neural crest migration (Rovasio and Battiato, 2002).…”

Section: Effects On Neural Crest Migrationmentioning

confidence: 99%

“…The cranial neural crest cells (CNCs) travel significantly shorter distances (50% of control values) and their migration is less directional, again with more retrograde movements (Rovasio and Battiato, 2002;Czarnobaj et al, 2014). At low ethanol (10.9 mM) only the migration of cranial populations was impaired (Czarnobaj et al, 2014), and it took substantially higher ethanol levels (150 mM) to impair trunk neural crest migration (Rovasio and Battiato, 2002). Importantly, this abnormal migration persisted for at least 24 hr following ethanol removal, suggesting that ethanol caused lasting changes in neural crest migratory capacity (Rovasio and Battiato, 2002).…”

Section: Effects On Neural Crest Migrationmentioning

confidence: 99%

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Neural crest development in fetal alcohol syndrome

Smith

Garic

Flentke

et al. 2014

Birth Defects Research Pt C

107

102

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Fetal alcohol spectrum disorder (FASD) is a leading cause of neurodevelopmental disability. Some affected individuals possess distinctive craniofacial deficits, but many more lack overt facial changes. An understanding of the mechanisms underlying these deficits would inform their diagnostic utility. Our understanding of these mechanisms is challenged because ethanol lacks a single receptor when redirecting cellular activity. This review summarizes our current understanding of how ethanol alters neural crest development. Ample evidence shows that ethanol causes the “classic” fetal alcohol syndrome (FAS) face (short palpebral fissures, elongated upper lip, deficient philtrum) because it suppresses prechordal plate outgrowth, thereby reducing neuroectoderm and neural crest induction and causing holoprosencephaly. Prenatal alcohol exposure (PAE) at premigratory stages elicits a different facial appearance, indicating FASD may represent a spectrum of facial outcomes. PAE at this premigratory period initiates a calcium transient that activates CaMKII and destabilizes transcriptionally active β-catenin, thereby initiating apoptosis within neural crest populations. Contributing to neural crest vulnerability are their low antioxidant responses. Ethanol-treated neural crest produce reactive oxygen species, and free radical scavengers attenuate their production and prevent apoptosis. Ethanol also significantly impairs neural crest migration, causing cytoskeletal rearrangements that destabilize focal adhesion formation; their directional migratory capacity is also lost. Genetic factors further modify vulnerability to ethanol-induced craniofacial dysmorphology, and include genes important for neural crest development including shh signaling, PDFGA, vangl2, and ribosomal biogenesis. Because facial and brain development are mechanistically and functionally linked, research into ethanol’s effects on neural crest also informs our understanding of ethanol’s CNS pathologies.

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Section: Effects On Neural Crest Migrationmentioning

confidence: 99%

Section: Effects On Neural Crest Migrationmentioning

confidence: 99%

Neural crest development in fetal alcohol syndrome

Smith

Garic

Flentke

et al. 2014

Birth Defects Research Pt C

107

102

View full text Add to dashboard Cite

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“…Prenatal ethanol exposure at a variety of developmental stages has been shown to disturb many aspects of neural crest development. Even low doses of ethanol exposure (equivalent to one drink) significantly altered the cellular activity of cranial and trunk neural crest cells from Xenopus embryos assayed in vitro (Czarnobaj et al, ). Two of the many mechanisms that may alter NCC number and migratory behavior are discussed next.…”

Section: Teratogens Disturb Neural Crest Cellsmentioning

confidence: 99%

Connecting teratogen‐induced congenital heart defects to neural crest cells and their effect on cardiac function

Karunamuni

et al. 2014

Birth Defects Research Pt C

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Neural crest cells play many key roles in embryonic development, as demonstrated by the abnormalities that result from their specific absence or dysfunction. Unfortunately, these key cells are particularly sensitive to abnormalities in various intrinsic and extrinsic factors, such as genetic deletions or ethanol-exposure that lead to morbidity and mortality for organisms. This review discusses the role identified for a segment of neural crest is in regulating the morphogenesis of the heart and associated great vessels. The paradox is that their derivatives constitute a small proportion of cells to the cardiovascular system. Findings supporting that these cells impact early cardiac function raises the interesting possibility that they indirectly control cardiovascular development at least partially through regulating function. Making connections between insults to the neural crest, cardiac function, and morphogenesis is more approachable with technological advances. Expanding our understanding of early functional consequences could be useful in improving diagnosis and testing therapies.

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“…In another study, cranial NCCs explants were exposed to low concentrations of ethanol. This treatment resulted in an initial delay in the number of NCCs emigrating from these explants, associated with a reduction in the overall distance covered by individual cells [42], again consistent with a role of ethanol in disrupting NCCs migration.…”

Section: Craniofacial Disorders Modeled In Xenopusmentioning

confidence: 65%

Modeling Human Craniofacial Disorders in Xenopus

Dubey

Saint-Jeannet

2017

Curr Pathobiol Rep

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Purpose of Review Craniofacial disorders are among the most common human birth defects and present an enormous health care and social burden. The development of animal models has been instrumental to investigate fundamental questions in craniofacial biology and this knowledge is critical to understand the etiology and pathogenesis of these disorders. Recent findings The vast majority of craniofacial disorders arise from abnormal development of the neural crest, a multipotent and migratory cell population. Therefore, defining the pathogenesis of these conditions starts with a deep understanding of the mechanisms that preside over neural crest formation and its role in craniofacial development. Summary This review discusses several studies using Xenopus embryos to model human craniofacial conditions, and emphasizes the strength of this system to inform important biological processes as they relate to human craniofacial development and disease.

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The different effects on cranial and trunk neural crest cell behaviour following exposure to a low concentration of alcohol in vitro

Cited by 18 publications

References 40 publications

Neural crest development in fetal alcohol syndrome

Neural crest development in fetal alcohol syndrome

Connecting teratogen‐induced congenital heart defects to neural crest cells and their effect on cardiac function

Modeling Human Craniofacial Disorders in Xenopus

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