Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Regulation of Fetal Liver Growth in a Model of Diet Restriction in the Pregnant Rat

ABSTRACT: The present study was designed to test the hypothesis that limited growth of the fetal liver in the model of maternal fasting is independent of well-characterized signaling mechanisms that are known to regulate somatic growth in adult animals. We profiled the fetal hepatic transcriptome and translatome in control (n=3) and IUGR (n=3) fetuses. To induce IUGR, pregnant dams were fasted for 48hr starting on E17, term being 21 days. Fetal rats were delivered by C-section and livers were removed. All livers were flash frozen in liquid nitrogen. RNA was extracted from polysomes that were generated using sucrose density fraction, as well as total liver. RNA was hybridized to Affymetrix GeneChip Rat Gene 1.0 ST Arrays.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Joan Boylan

PROVIDER: E-GEOD-77112 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Regulation of fetal liver growth in a model of diet restriction in the pregnant rat.

Boylan Joan M JM Sanders Jennifer A JA Gruppuso Philip A PA

American journal of physiology. Regulatory, integrative and comparative physiology 20160629 3

Limited nutrient availability is a cause of intrauterine growth restriction (IUGR), a condition that has important implications for the well being of the offspring. Using the established IUGR model of maternal fasting in the rat, we investigated mechanisms that control gene expression and mRNA translation in late-gestation fetal liver. Maternal fasting for 48 h during the last one-third of gestation was associated with a 10-15% reduction in fetal body weight and a disproportionate one-third redu ...[more]

PMID: 27357801

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Project description:Developmental exposures play a role in adult onset chronic disease. The mechanisms by which environmental toxicants alter developmental processes predisposing individuals to chronic disease are not understood. arsenic exposure via drinking water causes cancer and cardiovascular disease. Transplacental arsenic exposure accelerates and exacerbates atherosclerosis in ApoE-knockout mice. The liver plays a central role in the interlinked diseases diabetes, metabolic syndrome and atherosclerosis. The hypothesis that accelerated atherosclerosis is a consequence of altered hepatic development was investigated by microarray profiling of mRNA and microRNA abundance in livers isolated from 10 week old (PND70) and newborn (PND1) mice exposed or not exposed to arsenic from day 8 post-fertilization to birth. The results show that arsenic exposure alters the trajectory of both mRNA and microRNA expression as mice age. A 51-gene signature of arsenic exposure in both PND1 and PND70 mice was identified. Pathway Architect analysis of this signature identified nodes of interaction including Hspa8, IgM and Hnf4a. Gene ontology analysis of arsenic exposure-altered mRNAs indicated that pathways for gluconeogenesis and glycolysis were suppressed in PND1 mice and pathways for protein export, ribosome, antigen processing and presentation, and complement and coagulation cascades were induced in PND70 mice. Analysis of promoters of differentially expressed genes identified enriched transcription factor binding sites and cluster analyses revealed groups of genes sharing sets of transcription factor binding sites suggesting common regulation. Srebp1 binding sites are present in ~1/6 of the genes differentially expressed in PND70 livers. Western blot analyses of PND70 liver proteins showed that the inducible form of heat shock protein 70 (Hspa1, Hsp70) and the active form of Srebp1 were induced in arsenic-exposed mice as were plasma AST and ALT levels. These results suggest that transplacental ar Samples from three frozen livers from each group (newborn exposed and unexposed, 10 week old exposed and unexposed), and from separate litters, were homogenized and total RNA purified using mirVANA RNA pufification kits (Ambion, Carlsbad, CA). RNA was quantitated and intergrity determined on a Nanochip using a Bioanalyzer (Agilent, Santa Clara, CA). Microarray analyses for miRNAs abundance in total liver RNAs was performed by Exiqon (Woburn, MA) using two-color design against mouse standard total RNA (Ambion, now part of Applied Biosystems) and Exiqon LNA 1500 microarrays. Microarray analyses for mRNA abundance was performed using 2 color design against mouse standard total RNA (Stratgene, LaJolla, CA) and 44k arrays produced at the NIA . The processed data on Exiqon LNA-1500 are attached as a Series supplementary file. The data are based on the same samples as described in Agilent data submitted here. The supplementary data includes only the murine miRNA data on the array because these are the only data supplied by Exiqon. The relationship between GEO's sample names here (Agilent data) and column heads of spreadsheets (Exiqon data) are described in the first sheet of supplemental file: Project_Summary_Report_Heather_Miller_01042009_MTE.xls

Dataset Information

Regulation of Fetal Liver Growth in a Model of Diet Restriction in the Pregnant Rat

Publications

Regulation of fetal liver growth in a model of diet restriction in the pregnant rat.

Similar Datasets

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