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Table 1 Global gene expression studies after in utero alcohol exposure in mouse models

From: Genetic and epigenetic insights into fetal alcohol spectrum disorders

Alcohol exposure* Tissue Key upregulated genes/pathways Key downregulated genes/pathways Functional pathway References
(daily intraperitoneal dose 2.9 g/kg)
Fetal brain   Timp4, Bmp15, Rnf25, Tulp4 and Dexras1 Cell proliferation, cell differentiation and apoptosis; affecting tissue growth and remodeling and neural growth and survival [37]
(2 doses, 4 h apart, 2.9 g/kg)
Head fold, 3 h after alcohol exposure B6N: glycolysis and pentose phosphate pathway; B6J and B6N: tight junction, focal adhesion, adherens junction and regulation of the actin cytoskeleton B6N: ribosomal proteins and proteasome; B6J: none detected Common signaling pathways linking receptor activation to cytoskeletal reorganization [40]
for 46 h (peak alcohol concentration 88 mM)
Whole embryo culture All 3' miRNA motifs showed upregulatory effects Most 5' cis-acting regulatory motifs (transcription binding sites) showed down regulatory effects Developmental deficit of growth, neuronal axis and neural patterning, hemopoiesis and apoptosis [41]
for 46 h (peak alcohol concentration 88 mM)
Whole embryo culture Decreased methylation: Nlgn3, Elavl2, Sox 21, Sim1, Igf2r and Histh3d Increased methylation: Cyp4f13 Metabolism (Cyp4f13); imprinting (Igf2r); chromatin (Histh3d); and development (other genes) [38]
GD0.5-8.5 Liver from 28-day-old males D14ertd449e, Ly6e and Rrm2 Lima1, Socs2, Cables1 and Vidir Growth; nervous system development [39]
  1. *GD, gestational day. C57BL/6 substrains: B6J embryos had a higher incidence of FASD features than B6N. A possible interpretation is that many highly expressed genes were not appropriately downregulated because of delayed expression of miRNAs that would normally reduce expression.