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Expression data from PBDE-47 treated rats at PND4

ABSTRACT: To identify liver transcripts differentially expressed between control samples and animals exposed to PBDE-47, we collected RNA from male pups at postnatal day 4 (PND4) after the Wistar Han dams were exposed to 0, 0.1, 15, or 50 mg/kg PBDE-47. These samples were interrogated with the Affymetrix Rat Genome 230 2.0 GeneChip array. A total of 7, 50, and 149 gene transcripts were differentially expressed between control samples and 0.1, 15, and 50 mg/kg PBDE-47 (using a false discovery rate (FDR) threshold of 0.05). These transcripts were mapped to 2, 40, and 139 genes using Ingenuity Pathway Analysis.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE154912 | GEO | 2020/07/22

REPOSITORIES: GEO

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Project description:Polybrominated diphenyl ethers (PBDEs) were used as flame-retardant additives starting 1965 and were recently withdrawn from commerce in North America and Europe. Approximately 1/5 of the total U.S. population were born when environmental concentrations of PBDE plateaued at their maximum. Accumulating evidence suggests that developmental exposures to PBDE may result in long-lasting programming of liver metabolism. In this study, CD-1 mice were exposed prenatally or neonatally to 1 mg/kg body weight of 2,2’,4,4’-tetrabromodiphenyl ether (BDE-47), and changes in liver gene histology, transcriptome, and liver-blood balance of triglycerides were analyzed in 10 month old male offspring. In both exposure groups, long-term reprogramming of lipid metabolism was observed, including increased liver triglycerides and decreased blood triglycerides, and altered expression of metabolic genes in the liver. Significant upregulation of lipid influx transporter Cd36 2.3- and 5.7-fold in pre- and neonatal exposure groups respectively was identified as a potential mechanism of blood/liver imbalance of triglycerides. Analysis of our and previously published all-genome gene expression data identified changes in expression of ribosomal protein genes as a transcriptomic signature of PBDE exposure. Further comparison of our new data and published data demonstrate that low doses (0.2 mg/kg body weight) of PBDE induce long-lasting up-regulation of ribosomal genes, suppression of Cd36 in liver and increase circulating triglycerides in blood, while moderated doses (≥ 1 mg/kg body weight) produce opposite long-lasting effects. To conclude, this study shows that an environmentally relevant developmental exposures to BDE-47 permanently alter lipid uptake and accumulation in the liver, with low and moderate doses having opposite effect on liver transcriptomics and triglyceride balance. Similar effects of pre- and neonatal exposures point at hepatocyte maturation as a sensitive window of the liver metabolism programming. These results suggest that PBDE exposure may be an important factor increasing risks of cardio-vascular disease and non-alcoholic fatty liver disease. The translational relevance of these findings for human remain to be studied.

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Expression data from PBDE-47 treated rats at PND4

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