| Deciphering the role of Shh signaling in axial defects produced by ethanol exposure. | |
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MedLine Citation:
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PMID: 19235835 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: The phenotype of embryos exposed to ethanol is complex and likely due to multiple alterations in developmental pathways. We have previously demonstrated that Sonic hedgehog signaling (Shh-s) was reduced in both chicken and zebrafish embryos when exposed to ethanol. METHODS: There are many tissues affected by embryonic ethanol exposure, and in this article we explore the development of axial tissues, using zebrafish embryos. We then compare these effects to the phenotypes produced by exposure to two drugs that also inhibit Shh-s: cyclopamine and forskolin. RESULTS: We found alterations in the development of the notochord and somites produced by all three compounds, although only ethanol produced developmental delay of epiboly. Upon observation of early developing embryos, muscle pioneer cells were completely lost in cyclopamine-treated embryos, and reduced, but less so, in embryos treated with forskolin and ethanol. Ethanol treatment produced a dose-dependent reduction in total body length that may be linked to epiboly delay seen earlier during development. Despite the differences between cyclopamine and forskolin, we found that shh mRNA injection rescued the short body length, the alteration in somite shape, and the cyclopia produced by ethanol exposure. CONCLUSIONS: Taken together, each teratogen produced a unique set of phenotypic changes in the body axis, suggesting that each compound affects Shh-s and also produces a distinctive set of molecular alterations. However, addition of exogenous Shh to ethanol treated zebrafish prevented many of the gross physical phenotypes, suggesting that the suppression of Shh-s is one of the major effects of ethanol exposure. |
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Authors:
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Evyn J Loucks; Sara C Ahlgren |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Birth defects research. Part A, Clinical and molecular teratology Volume: 85 ISSN: 1542-0760 ISO Abbreviation: Birth Defects Res. Part A Clin. Mol. Teratol. Publication Date: 2009 Jun |
Date Detail:
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Created Date: 2009-06-15 Completed Date: 2009-08-18 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101155107 Medline TA: Birth Defects Res A Clin Mol Teratol Country: United States |
Other Details:
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Languages: eng Pagination: 556-67 Citation Subset: IM |
Affiliation:
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Children's Memorial Research Center Program in Developmental Biology, Chicago, Illinois 60640, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Central Nervous System Depressants / pharmacology, toxicity Dose-Response Relationship, Drug Embryo, Nonmammalian / metabolism Embryonic Development / drug effects* Ethanol / pharmacology, toxicity* Hedgehog Proteins / metabolism* Notochord / embryology* Signal Transduction / drug effects* Teratogens / pharmacology, toxicity* Zebrafish / embryology* Zebrafish Proteins / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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R21 AA13596/AA/NIAAA NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Central Nervous System Depressants; 0/Hedgehog Proteins; 0/Teratogens; 0/Zebrafish Proteins; 64-17-5/Ethanol |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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