Sonic hedgehog rescues cranial neural crest from cell death induced by ethanol exposure

Ahlgren, Sara; Thakur, Vijaya; Bronner‐Fraser, Marianne

doi:10.1073/pnas.162356199

Cited by 221 publications

(229 citation statements)

References 31 publications

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“…The evidence presented here and elsewhere 38,65 consistently demonstrates that fetal alcohol exposure inhibits the transcription of Shh responsive genes. Notably, we found that total Shh protein level in the zebrafish embryonic tissues was not significantly changed by any of the tested alcohol exposures.…”

Section: Discussionsupporting

confidence: 77%

“…This findings help to explain why over-expression of Shh mRNA alone does not consistently rescue alcohol-induced morphologic defects or the decrease in expression of Shh responsive genes. 38,65 Here, we observed that supplementing a simple chemical, cholesterol rescues the alcohol-inhibited Hh signal transduction and prevents embryos from developing FASD-like morphologic defects. Recently, sterols were shown to directly activate the Shh signaling pathway through Smo.…”

Section: Discussionmentioning

confidence: 87%

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Fetal alcohol exposure impairs hedgehog cholesterol modification and signaling

Yang

Zdanowicz

et al. 2007

Laboratory Investigation

135

144

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 87%

Fetal alcohol exposure impairs hedgehog cholesterol modification and signaling

Yang

Zdanowicz

et al. 2007

Laboratory Investigation

135

144

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“…Ahlgren and Bronner-Fraser (1999) showed that inhibition of Shh in the cranial mesenchyme also caused neural crest mesenchymal cell death. Moreover, Ahlgren et al (2002) demonstrated that application of Shh protein rescued cranial mesenchymal death in chick embryos induced by ethanol treatment. These data indicate that Shh signaling is required for facial mesenchyme survival.…”

Section: The Shh Pathwaymentioning

confidence: 99%

Development of the upper lip: Morphogenetic and molecular mechanisms

Jiang

Bush

Lidral

2005

Developmental Dynamics

288

304

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The vertebrate upper lip forms from initially freely projecting maxillary, medial nasal, and lateral nasal prominences at the rostral and lateral boundaries of the primitive oral cavity. These facial prominences arise during early embryogenesis from ventrally migrating neural crest cells in combination with the head ectoderm and mesoderm and undergo directed growth and expansion around the nasal pits to actively fuse with each other. Initial fusion is between lateral and medial nasal processes and is followed by fusion between maxillary and medial nasal processes. Fusion between these prominences involves active epithelial filopodial and adhering interactions as well as programmed cell death. Slight defects in growth and patterning of the facial mesenchyme or epithelial fusion result in cleft lip with or without cleft palate, the most common and disfiguring craniofacial birth defect. Recent studies of craniofacial development in animal models have identified components of several major signaling pathways, including Bmp, Fgf, Shh, and Wnt signaling, that are critical for proper midfacial morphogenesis and/or lip fusion. There is also accumulating evidence that these signaling pathways cross-regulate genetically as well as crosstalk intracellularly to control cell proliferation and tissue patterning. This review will summarize the current understanding of the basic morphogenetic processes and molecular mechanisms underlying upper lip development and discuss the complex interactions of the various signaling pathways and challenges for understanding cleft lip pathogenesis.

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“…78 Work in chicken, mouse, and zebrafish has shown that ethanol exposure reduces Shh signaling leading to increased CNCC death, as well as disrupted midline and eye development. 30,[79][80][81][82] These ethanol-induced phenotypes can be rescued by injection of shh mRNA. 50 In addition to altering retinoic acid signaling, one alternative (or additional) mechanism by which ethanol attenuates Shh is the disruption of cholesterol modification of Shh needed for proper signaling, as has been found in zebrafish.…”

Section: Zebrafish Models Of Fasdmentioning

confidence: 99%

Fishing for Fetal Alcohol Spectrum Disorders: Zebrafish as a Model for Ethanol Teratogenesis

2016

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Fetal Alcohol Spectrum Disorders (FASD) describes a wide array of ethanol-induced developmental defects, including craniofacial dysmorphology and cognitive impairments. It affects *1 in 100 children born in the United States each year. Due to the pleiotropic effects of ethanol, animal models have proven critical in characterizing the mechanisms of ethanol teratogenesis. In this review, we focus on the utility of zebrafish in characterizing ethanolinduced developmental defects. A growing number of laboratories have focused on using zebrafish to examine ethanol-induced defects in craniofacial, cardiac, ocular, and neural development, as well as cognitive and behavioral impairments. Growing evidence supports that genetic predisposition plays a role in these ethanol-induced defects, yet little is understood about these gene-ethanol interactions. With a high degree of genetic amenability, zebrafish is at the forefront of identifying and characterizing the gene-ethanol interactions that underlie FASD.

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Sonic hedgehog rescues cranial neural crest from cell death induced by ethanol exposure

Cited by 221 publications

References 31 publications

Fetal alcohol exposure impairs hedgehog cholesterol modification and signaling

Fetal alcohol exposure impairs hedgehog cholesterol modification and signaling

Development of the upper lip: Morphogenetic and molecular mechanisms

Fishing for Fetal Alcohol Spectrum Disorders: Zebrafish as a Model for Ethanol Teratogenesis

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