title: Gene expression changes of sonic hedgehog signaling cascade in a mouse embryonic model of fetal alcohol syndrome.
abstract: Fetal alcohol syndrome (FAS) is a congenital anomaly attributable to prenatal maternal excessive intake of ethanol. The authors made a mammalian model of FAS by culturing mouse embryos with high ethanol for embryonic day 7.8 to 9.5 in the whole embryo culture system. The embryos exposed to high ethanol were smaller and less advanced in development than were the embryos in the control group and showed craniofacial abnormalities, such as a fusion defect of the neural tube. The expression patterns of CRABP-I and AP-2 as markers of the neural crest cells were mostly unchanged in the in situ hybridization. However, the density and area of the expression were decreased, possibly because of the death of the neural crest cells. The expression patterns of the Sonic hedgehog signaling cascade genes (Shh, Ptc-1 and Gli-1) were mostly unchanged in the in situ hybridization, but the quantitative expressions of Ptc-1 and Gli-1 were increased in real-time reverse transcriptase-polymerase chain reaction analyses, quite contrary to the findings of a previous study using chick embryos. These findings suggest Shh signaling also is involved in the pathogenesis of FAS in mammalian embryo, but in a mode different from that in the chick embryo.
authors.affiliation: Department of Plastic and Reconstructive Surgery, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
authors.forename: Yoko
authors.initials: Y
authors.lastname: Yamada
authors.forename: Takashi
authors.initials: T
authors.lastname: Nagase
authors.forename: Miki
authors.initials: M
authors.lastname: Nagase
authors.forename: Isao
authors.initials: I
authors.lastname: Koshima
mesh_terms: D000818:Animals; D019465:Craniofacial Abnormalities / Q000196:embryology / Q000235:genetics; D004195:Disease Models, Animal; D046149:Embryo Culture Techniques; D047108:Embryonic Development / Q000235:genetics; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000235:genetics*; D005786:Gene Expression Regulation / Q000235:genetics*; D053823:Hedgehog Proteins; D017403:In Situ Hybridization; D051741:Kruppel-Like Transcription Factors / Q000235:genetics; D051379:Mice; D008813:Mice, Inbred ICR; D009436:Neural Tube Defects / Q000196:embryology / Q000235:genetics; D000072079:Patched Receptors; D000072081:Patched-1 Receptor; D011247:Pregnancy; D011956:Receptors, Cell Surface / Q000235:genetics; D018168:Receptors, Retinoic Acid / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000235:genetics*; D015534:Trans-Activators / Q000235:genetics*; D050656:Transcription Factor AP-2 / Q000235:genetics; D000071676:Zinc Finger Protein GLI1
chemical_list: C498520:Gli1 protein, mouse; D053823:Hedgehog Proteins; D051741:Kruppel-Like Transcription Factors; D000072079:Patched Receptors; D000072081:Patched-1 Receptor; C000606240:Ptch1 protein, mouse; D011956:Receptors, Cell Surface; D018168:Receptors, Retinoic Acid; C465570:Shh protein, mouse; D015534:Trans-Activators; D050656:Transcription Factor AP-2; D000071676:Zinc Finger Protein GLI1; C082927:retinoic acid binding protein I, cellular