Rat gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA291923 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2179743.fastq.gz | Fastqsanger.gz | |||
| SRR2179744.fastq.gz | Fastqsanger.gz | |||
| SRR2179738.fastq.gz | Fastqsanger.gz |
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Project description:Analysis of gut microbiota by pyrosequencing of 16S rRNA gene in F344 rats
| PRJNA280958 | ENA
Project description:When applied in toxicological studies, the recently developed gene expression profiling techniques using microarrays, which brought forth the new field of toxicogenomics, facilitate the interpretation of a toxic compound?s mechanism of action. In this study, we investigated whether genotoxic carcinogens at doses known to induce liver tumors in the 2-year rat bioassay deregulate a common set of genes in a short-term in vivo study and, if so, whether these deregulated genes represent defined biological pathways. Rats were dosed with the four genotoxic hepatocarcinogens Dimethylnitrosamine [CAS:62-75-9;CHEBI:21778] (4 mg/kg/day), 2-nitrofluorene [CAS:607-57-8;CHEBI:1224] (44 mg/kg/day), Aflatoxin B1 [CAS:1162-65-8;CHEBI:2504] (0.24 mg/kg/day), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone [CAS:64091-91-4;CHEBI:32692] (NNK, 20 mg/kg/day). After treatment for up to 14 days, the expression profiles of the livers were analyzed on Affymetrix RG_U34A microarrays. Among the significantly upregulated genes were a set of target genes of the tumor suppressor protein p53, indicating a DNA damage response. Such a response was expected and, therefore, confirmed the validity of our approach. In addition, the gene expression changes suggest a specific detoxification response, the activation of proliferative and survival signaling pathways, and some cell structural changes. These responses were strong throughout the 14 day time course for 2-nitrofluorene and aflatoxin B1; in the case of dimethylnitrosamine and NNK, the effects were weakly detectable at day 1 and then increased with time. For dimethylnitrosamine and aflatoxin B1, which caused observable inflammation in vivo, we found a corresponding upregulation of inflammatory genes at the same time points. Thus, by the toxicogenomic analysis of short-term in vivo studies, we identified genes and pathways commonly deregulated by genotoxic carcinogens, which may be indicative for the early events in tumorigenesis and, thus, predictive of later tumor development.
2005-05-15 | E-TOXM-16 | biostudies-arrayexpress
Project description:Chronic acid suppression by proton pump inhibitor (PPI) has been hypothesized to alter the gut microbiota via a change in intestinal pH. To evaluate the changes in gut microbiota composition by long-term PPI treatment. Twenty-four week old F344 rats were fed with (n = 5) or without (n = 6) lansoprazole (PPI) for 50 weeks. Then, profiles of luminal microbiota in the terminal ileum were analyzed. Pyrosequencing for 16S rRNA gene was performed by genome sequencer FLX (454 Life Sciences/Roche) and analyzed by metagenomic bioinformatics.
2015-04-14 | E-GEOD-67800 | biostudies-arrayexpress
Project description:Susceptibility to the hepatocarcinogen Aflatoxin B1 (AFB1) varies among species and with age. Mice are refractory to carcinogenic and toxic effects of AFB1; however, B6C3F1 mice show transient sensitivity if dosed shortly after birth. We compared age-related differences in gene expression and transcriptional responses to AFB1 in livers of newborn (4-day-old) and adult mice. Keywords: Transcriptional response to a carcinogen
2009-01-01 | GSE4740 | GEO
Project description:Predisposition to hepatocarcinogenesis is under polygenic control. We analyzed gene expression patterns of dysplastic liver nodules (DN) and hepatocellular carcinoma (HCC) chemically-induced in F344 and BN rats, respectively susceptible and resistant to hepatocarcinogenesis, to evaluate effector mechanisms of predisposition genes, and commonalties between transcription signatures of rat and human liver lesions. Gene expression profiles were determined by microarray analysis and validated by quantitative RT-PCR and Western blot. Cluster analysis revealed two distinctive gene expression patterns, the first of which included normal liver of F344 and BN rats and BN rat nodules, and the second one F344 nodules and HCC of both strains. Expression of 91 and 55 genes of DN and HCC, respectively, showed significant interstrain differences. Considering genes mostly associated with cell proliferation we identified a signature predicting DN evolution to HCC. Notably, expression of oncosuppressors Csmd1, Dmbt, Dusp1, and Gnmt ,in DN, and Bhmt, Dmbt1, Dusp1, Gadd45g, Gnmt, Napsa, Pp2ca, and Ptpn13, in HCC, was higher in BN than F344 rats. Comparative genomics approach, using gene expression data from rat lesions, and human HCC with different prognosis (based on survival length), revealed expression patterns of BN and F344 lesions close to those of human HCCs with better and poorer prognosis, respectively, suggesting that similar molecular events contribute to create a phenotype prone to progression in rats and human lesions. In conclusion, we identified a molecular signature of DN prone to progress to HCC and suggest that oncosuppressor genes are determinants of the genetically transmitted resistance to hepatocarcinogenesis.
2010-10-09 | GSE24600 | GEO
Project description:In order to gain insight into the effects of aging on susceptibility to environmental toxins, we characterized the expression of xenobiotic metabolizing enzymes (XMEs) from the livers of male Brown Norway and F344 rats across the adult lifespan. To examine metabolic processes across lifespan after challenge with a xenobiotic compound, Brown Norway rats were exposed to 1.0 g/kg body weight toluene by oral gavage in corn oil (4ml/kg body weight) or corn oil alone. Experiment Overall Design: Brown Norway rats: Analysis of gene expression profiles for XMEs in male Brown Norway rats 4, 12, and 24 months old. Rats were exposed to 1g/kg toluene by oral gavage, and sacrificed after 4 hours. Total RNA was isolated from liver samples and gene expression analyzed using Affymetrix Rat 230 2.0 full-genome GeneChips. Data from 18 samples, with three rats in each of the control age groups and dosed age groups, were analyzed. Experiment Overall Design: F344 rats: Analysis of gene expression profiles for XMEs in male F344 6, 11, 18, and 24 months old. Total RNA was isolated from liver samples and gene expression analyzed using Affymetrix Rat 230 2.0 full-genome GeneChips. Data from 16 samples, with four rats in each of the 4 age groups, were analyzed.
2008-10-20 | E-GEOD-11097 | biostudies-arrayexpress
Project description:Thy1 + cells isolated from male F344 rats with Dgalactosamine-induced liver injury were cultured for one week. Bone marrow mesenchymal cells isolated from from the femurs and tibias of a 5-week old male F344 rat. Small hepatocytes (SH) and mature hepatocytes (MH) were isolated from normal livers of 7-week old male F344 rat, Extracellular vesicles (EVs) were separedt from culture media by ultracentrifugation.
2023-04-07 | GSE222517 | GEO
Project description:At present, substantial efforts are focused on the development of in vitro assays coupled with M-bM-^@M-^]omicsM-bM-^@M-^] technologies for the identification of carcinogenic substances as an alternative to the classical 2-year rodent carcinogenicity bioassay. A prerequisite for the eventual regulatory acceptance of such assays, however, is the in vivo relevance of the observed in vitro findings. In the current study, hepatocarcinogen-induced gene expression profiles generated after exposure of conventional cultures of primary rat hepatocytes to three non-genotoxic carcinogens (methapyrilene hydrochloride, piperonyl butoxide and Wy-14643), three genotoxic carcinogens (aflatoxin B1, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and 2-nitrofluorene), and two non-carcinogens (nifedipine and clonidine) are compared with previously obtained in vivo data after oral administration for up to 14 days of the same hepatocarcinogens to rats.
2012-04-23 | E-GEOD-36524 | biostudies-arrayexpress
Project description:The industrial solvent trichloroethylene (TCE) produces a marked formic aciduria in male and female F344 rats and in male C57Bl mice following single or multiple dosing. The two major metabolites of TCE formed by cytochromes P450 metabolism also produce formic aciduria. The quantity of formic acid excreted was about 2-fold higher following trichloroacetic acid (TCA) compared to trichloroethanol (TCE-OH) or TCE, at similar doses of 16mg/kg/day for 3 days. Prior treatment of male F344 rats with 1-aminobenzotriazole a cytochrome P450 inhibitor, followed by TCE, completely prevented the formic aciduria but had no effect on formic acid excretion produced by TCA, suggesting TCA is the proximate metabolite producing this response. Metabolism of formic acid is largely controlled by the vitamin B12 –dependent methionine salvage pathway. Transcriptomic analysis on the liver of rats dosed with 16mg/kg/day TCE for three days when compared to control liver showed nine differentially expressed genes, of particular interest was the down regulation of LMBRD1 involved in the conversion of vitamin B12 into one of two molecules, methylcobalamin (CH3Cbl) or S-adenosylcobalamin (AdoCbl). Administration of CH3Cbl or hydroxocobalamin for 3 days to rats given a single dose of TCE, lead to a reduction in formic acid in their urine. Similarly, rats given TCE followed by L-methionine for 3 days excreted less formic acid in their urine. These findings suggest an effect on the vitamin B12 –dependent methionine salvage pathway. This was supported by the finding that hepatic methionine synthase, which converts homocysteine to methionine, was inhibited following three large daily dose of TCE. We propose that TCE metabolites interact with the vitamin B12 -dependent methionine salvage pathway leading to tetrahydrofolate deficiency and increased excretion of formic acid in rat urine.
2020-11-20 | GSE122664 | GEO
Project description:Fecal samples collected on day 5 from randomly selected colitic SD rats were analyzed for gut microbiota by sequencing the V4 region of the 16S rRNA gene. The orally administered Dex-P-laden NPA2 coacervate (Dex-P/NPA2) significantly restores the diversity of gut microbiota compared with colitic SD rats in the Dex-P/PBS group and the untreated colitic rats (Control).
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