Rattus norvegicus
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PROVIDER: PRJNA265190 | ENA |
REPOSITORIES: ENA
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Project description:Toxicogenomic Assessment of Liver Responses following subchronic exposure to furan in Fischer F344 rats [cRNA]
| PRJNA265190 | ENA
Project description:Toxicogenomic Assessment of Liver Responses following subchronic exposure to furan in Fischer F344 rats
| PRJNA265192 | ENA
Project description:Toxicogenomic Assessment of Liver Responses following subchronic exposure to furan in Fischer F344 rats [miRNA]
| PRJNA265191 | ENA
Project description:The carcinogenic effect of furan, a potent hepatotoxicant and rodent liver carcinogen, has been attributed to genotoxic and non-genotoxic, including epigenetic, changes in the liver; however, the mechanisms of the furan liver tumorigenicity are still unclear. The goal of the present study was to investigate the role of transcriptomic and epigenetic events in the development of hepatic lesions in Fischer (F344) rats induced by furan treatment in a classic two-year rodent tumorigenicity bioassay. Male F344 rats were distributed randomly into control and experimental groups. Rats from the experimental groups were treated by gavage 5 days/week with either 0.92 or 2.0 mg furan/kg body weight (bw) in corn oil for 104 weeks. Rats from control group received corn oil only. High-throughput whole genome microarray analyses demonstrated distinctive dose-dependent alterations in gene expression in the furan-induced liver lesions. A total of 2073 and 2422 genes was found to be differentially expressed in the furan-induced liver lesions in rats treated with 0.92 and 2.0 mg furan/kg bw, respectively, as compared to normal liver tissue. Approximately 60% (1340) of the differentially expressed genes were common to both treatment groups. In silico analysis of the common differentially expressed genes revealed the presence of CpG island in 51% (679) of the genes, suggesting that they may be epigenetically regulated. Promoter methylation analysis of individual differentially expressed CpG island-containing genes demonstrated dose-dependent gene-specific methylation changes that were highly correlated with gene expression. Our findings illustrate that gene-specific DNA methylation changes have functional consequences and may contribute to the development of furan-induced pathologic liver lesions.
2015-07-18 | GSE71055 | GEO
Project description:Samples were the retrosplenial cortex dissected from female Fischer F344 rats that were 3-, 12-, or 23 months old.
2024-08-01 | PXD051203 | Pride
Project description:Transcriptomic data obtained by RNA-seq from male Fischer 344 rats treated with furan and 3-methylfuran were compared and contrasted. Microarray data from the same rats treated with furan was also used to compare microarray to RNA seq analysis.
2024-01-08 | GSE249626 | GEO
Project description:We profiled hepatic transcriptional responses of 6 strains of rats with varying sensitivity to a dioxin, TCDD, at 19 hours following exposure. The resistant rats exhibited significantly reduced transcriptional responses in comparison to the sensitive strains. We hypothesize that genes which show differential changes between the resistant and sensitive rats may potentially explain sensitivity. Rats with varying sensitivities (Long-Evans, L-E; Han/Wistar, H/W; Fischer 344, F344; Wistar, Wis; Line-A, Ln-A; and Line-C, Ln-C) were treated with 100 ug/kg TCDD or corn oil vehicle and euthanized 19 hours post-treatment. Each treatment group contains four or six animals (biological replicates), each of which was assayed on an individual microarray.
2011-08-16 | E-GEOD-31411 | biostudies-arrayexpress
Project description:To provide insights into the mode of action for Ni3S2 lung carcinogenicity by examining gene expression changes in target cells after inhalation exposure. Gene expression changes were determined in micro-dissected lung broncho-alveolar cells from Fischer F344 rats following inhalation of Ni3S2 at 0.0, 0.04, 0.08, 0.15, and 0.60 mg/m3 (0.03, 0.06, 0.11, and 0.44 mg Ni/m3) for one and four weeks (6 hours per day, 5 days per week). Results: Broncho-alveolar lavage fluid evaluation and lung histopathology provided evidence of inflammation only at the two highest concentrations, which were similar to those tested in the 2-year bioassay. The number of statistically significant up- and down-regulated genes decreased markedly from one to four weeks of exposure, suggesting adaptation. Cell signal pathway enrichment at both time-points primarily reflected responses to toxicity, including inflammatory and proliferative signaling. While proliferative signaling was up-regulated at both time points, some inflammatory signaling reversed from down-regulation at 1 week to up-regulation at 4 weeks. Conclusions: These results support a mode of action for Ni3S2 carcinogenicity driven by chronic toxicity, inflammation and proliferation, leading to mis-replication, rather than by direct genotoxicity. Benchmark dose (BMD) analysis identified the lowest pathway transcriptional BMD exposure concentration as 0.026 mg Ni/m3, for apoptosis/survival signaling. When conducted on the basis of lung Ni concentration the lowest pathway BMD was 0.64 M-BM-5g Ni/g lung, for immune/inflammatory signaling. Implications: These highly conservative BMDs could be used to derive a point of departure in a nonlinear risk assessment for Ni3S2 toxicity and carcinogenicity. Gene expression changes were determined in micro-dissected lung broncho-alveolar cells from Fischer F344 rats following inhalation of Ni3S2 at 0.0, 0.04, 0.08, 0.15, and 0.60 mg/m3 (0.03, 0.06, 0.11, and 0.44 mg Ni/m3) for one and four weeks (6 hours per day, 5 days per week).
2014-07-19 | E-GEOD-59593 | biostudies-arrayexpress
Project description:Furan is a heterocyclic organic compound produced in the chemical manufacturing industry and also found in a broad range of food products, including infant formulas and baby foods. Previous reports have indicated that the adverse biological effects of furan, including its liver tumorigenicity, may be associated with epigenetic abnormalities. In the present study we investigated the persistence of epigenetic alterations in rat liver. Male Fisher 344 (F344) rats were treated by gavage 5 days per week with 8 mg furan/kg body weight (bw)/day for 90 days. After the last treatment, rats were divided randomly into four groups; one group of rats was sacrificed 24 hours after the last treatment, while other groups were maintained without further furan treatment for an additional 90, 180, or 360 days. Treatment with furan for 90 days resulted in alterations in histone lysine methylation and acetylation, oxidative damage to DNA, and changes in the gene expression in the livers. A majority of these furan-induced molecular changes was transient and disappeared after the cessation of furan treatment. In contrast, histone H3 lysine 9, H3 lysine 27, and H3 lysine 56 showed a sustained and time-depended decrease in acetylation, which was associated with formation of heterochromatin and altered gene expression. These results indicate that furan-induced adverse effects may be mechanistically related to sustained changes in histone lysine acetylation that compromise the ability of cells to maintain and control properly the expression of genetic information.
2014-12-02 | GSE63740 | GEO
Project description:Different inbred strains of rats differ in their susceptibility to OIR, an animal model of human retinopathy of prematurity. We examined gene expression profiles in Fischer 344 (F344, resistant to OIR) and Sprague Dawley (SD, susceptible to OIR) rats at the early time point of day 3 to identifying gene pathways related to the underlying genetic cause of phenotypic differences between strains.
2009-11-13 | GSE18998 | GEO