Transcriptomics

Dataset Information

5

Postnatal Growth Restriction and Gene Expression Changes in a Mouse Model of Fetal Alcohol Syndrome (Kidney)


ABSTRACT: Growth restriction, craniofacial dysmorphology and central nervous system defects are the main diagnostic features of fetal alcohol syndrome. Studies in humans and mice have reported that the growth restriction can be prenatal and/or postnatal, but the underlying mechanisms remain unknown. We recently described a mouse model of moderate gestational ethanol exposure that produces measurable phenotypes in line with fetal alcohol syndrome, e.g. craniofacial changes and growth restriction in adolescent mice. Here we further characterize the growth restriction phenotype by measuring body weight at gestational day 16.5, cross-fostering from birth to weaning, and extending our observations into adulthood. Furthermore, in an attempt to unravel the molecular events contributing to the growth phenotype, we have compared gene expression patterns in the liver and kidney of non-fostered ethanol-exposed and control mice at postnatal day 28. We find that the ethanol-induced growth phenotype is not detectable prior to birth, but is present at weaning, even in mice that have been cross-fostered to unexposed dams. This suggests a postnatal growth restriction phenotype that is not due to deficient postpartum care by dams that drank ethanol, but rather a physiological result of ethanol exposure in utero. We also find that, despite some catch-up growth after five weeks of age, the effect extends into adulthood, consistent with longitudinal studies in humans. Genome-wide gene expression analysis revealed interesting ethanol-induced changes in the liver, including genes involved in the metabolism of exogenous and endogenous compounds, iron homeostasis and lipid metabolism. Gene expression changes in the kidneys of offspring exposed to alcohol in utero compared to controls.

ORGANISM(S): Mus musculus  

SUBMITTER: Suyinn Chong  

PROVIDER: E-GEOD-23105 | ArrayExpress | 2010-10-01

SECONDARY ACCESSION(S): GSE23105PRJNA133229

REPOSITORIES: GEO, ArrayExpress

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Publications

Postnatal growth restriction and gene expression changes in a mouse model of fetal alcohol syndrome.

Kaminen-Ahola Nina N   Ahola Arttu A   Flatscher-Bader Traute T   Wilkins Sarah J SJ   Anderson Greg J GJ   Whitelaw Emma E   Chong Suyinn S  

Birth defects research. Part A, Clinical and molecular teratology 20101001 10


Growth restriction, craniofacial dysmorphology, and central nervous system defects are the main diagnostic features of fetal alcohol syndrome. Studies in humans and mice have reported that the growth restriction can be prenatal or postnatal, but the underlying mechanisms remain unknown.We recently described a mouse model of moderate gestational ethanol exposure that produces measurable phenotypes in line with fetal alcohol syndrome (e.g., craniofacial changes and growth restriction in adolescent  ...[more]

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