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Series GSE23105 Query DataSets for GSE23105
Status Public on Oct 01, 2010
Title Postnatal Growth Restriction and Gene Expression Changes in a Mouse Model of Fetal Alcohol Syndrome (Kidney)
Organism Mus musculus
Experiment type Expression profiling by array
Summary 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.
 
Overall design Gene expression changes in the kidneys of offspring exposed to alcohol in utero compared to controls.
 
Contributor(s) Chong S
Citation(s) 20878912
Submission date Jul 23, 2010
Last update date Jan 16, 2019
Contact name Suyinn Chong
Organization name Queensland Institute of Medical Research
Department Division of Genetics and Population Health
Lab Epigenetics Laboratory
Street address 300 Herston Rd
City Herston
State/province Queensland
ZIP/Postal code 4006
Country Australia
 
Platforms (1)
GPL6887 Illumina MouseWG-6 v2.0 expression beadchip
Samples (12)
GSM569369 kidney_control_rep1
GSM569370 kidney_control_rep2
GSM569371 kidney_control_rep3
This SubSeries is part of SuperSeries:
GSE23115 Postnatal Growth Restriction and Gene Expression Changes in a Mouse Model of Fetal Alcohol Syndrome
Relations
BioProject PRJNA133229

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE23105_RAW.tar 15.8 Mb (http)(custom) TAR
GSE23105_kidney_non-normalized.txt.gz 3.4 Mb (ftp)(http) TXT
Processed data included within Sample table

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