{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T06:45:57Z","timestamp":1790145957241,"version":"4.0.1"},"reference-count":52,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2012,4,24]],"date-time":"2012-04-24T00:00:00Z","timestamp":1335225600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp; Exp Res"],"published-print":{"date-parts":[[2012,9]]},"abstract":"Background<\/jats:title>Prenatal alcohol exposure can result in fetal alcohol spectrum disorders (FASD<\/jats:styled-content>). Not all women who consume alcohol during pregnancy have children with FASD<\/jats:styled-content> and studies have shown that genetic factors can play a role in ethanol teratogenesis. We examined gene expression in embryos and placentae from C<\/jats:styled-content>57BL<\/jats:styled-content>\/6J (B<\/jats:styled-content>6) and DBA<\/jats:styled-content>\/2J<\/jats:styled-content> (D<\/jats:styled-content>2) mice following prenatal alcohol exposure. B<\/jats:styled-content>6 fetuses are susceptible to morphological malformations following prenatal alcohol exposure while D<\/jats:styled-content>2 are relatively resistant.<\/jats:p><\/jats:sec>Methods<\/jats:title>Male and female B<\/jats:styled-content>6 and D<\/jats:styled-content>2 mice were mated for 2\u00a0hours in the morning, producing 4 embryonic genotypes: true\u2010bred B<\/jats:styled-content>6B<\/jats:styled-content>6 and D<\/jats:styled-content>2D<\/jats:styled-content>2, and reciprocal B<\/jats:styled-content>6D<\/jats:styled-content>2 and D<\/jats:styled-content>2B<\/jats:styled-content>6. On gestational day 9, dams were intubated with 5.8\u00a0g\/kg ethanol, an isocaloric amount of maltose dextrin, or nothing. Four hours later, dams were sacrificed and embryos and placentae were harvested. RNA<\/jats:styled-content> was extracted, labeled and hybridized to A<\/jats:styled-content>ffymetrix M<\/jats:styled-content>ouse G<\/jats:styled-content>enome 430 v2 microarray chips. Data were normalized, subjected to analysis of variance and tested for enrichment of gene ontology molecular function and biological process using the D<\/jats:styled-content>atabase for A<\/jats:styled-content>nnotation, V<\/jats:styled-content>isualization and I<\/jats:styled-content>ntegrated D<\/jats:styled-content>iscovery (DAVID<\/jats:styled-content>).<\/jats:p><\/jats:sec>Results<\/jats:title>Several gene classes were differentially expressed in B<\/jats:styled-content>6 and D<\/jats:styled-content>2 regardless of treatment, including genes involved in polysaccharide binding and mitosis. Prenatal alcohol exposure altered expression of a subset of genes, including genes involved in methylation, chromatin remodeling, protein synthesis, and mRNA<\/jats:styled-content> splicing. Very few genes were differentially expressed between maltose\u2010exposed tissues and tissues that received nothing, so we combined these groups for comparisons with ethanol. While we observed many expression changes specific to B<\/jats:styled-content>6 following prenatal alcohol exposure, none were specific for D<\/jats:styled-content>2. Gene classes up\u2010 or down\u2010regulated in B6 following prenatal alcohol exposure included genes involved in mRNA<\/jats:styled-content> splicing, transcription, and translation.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>Our study identified several classes of genes with altered expression following prenatal alcohol exposure, including many specific for B<\/jats:styled-content>6, a strain susceptible to ethanol teratogenesis. Lack of strain specific effects in D<\/jats:styled-content>2 suggests there are few gene expression changes that confer resistance. Future studies will begin to analyze functional significance of the expression changes.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1530-0277.2012.01757.x","type":"journal-article","created":{"date-parts":[[2012,4,24]],"date-time":"2012-04-24T23:33:08Z","timestamp":1335310388000},"page":"1519-1529","source":"Crossref","is-referenced-by-count":53,"title":["Gene Expression Changes in C<\/scp>57BL<\/scp>\/6J<\/scp> and DBA<\/scp>\/2J<\/scp> Mice Following Prenatal Alcohol Exposure"],"prefix":"10.1111","volume":"36","author":[{"given":"Chris","family":"Downing","sequence":"first","affiliation":[{"name":"Department of Biomedical and Pharmaceutical Sciences College of Pharmacy Idaho State University Pocatello Idaho"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen","family":"Flink","sequence":"additional","affiliation":[{"name":"Department of Pharmacology University of Colorado School of Medicine Aurora 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