Inhalation exposure of hexanal in rats (mRNA)
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
SUBMITTER: Yoon Cho
PROVIDER: E-GEOD-60118 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:To further development of insight into the mechanism of toxicity, it is important to employ whole genome microarray expression profiling to identify and characterize miRNAs profiles as a discovery platform relevant for toxicologic mechanisms of hexanal. miRNAs have prominent role in cell cycle control, apoptosis, cancer development and proliferation-related processes. However, few reports have described the effect of hexanal on miRNA expression profiles using animal model. In this respect, we studied the expression profiles of miRNAs in hexanal-exposed in rats by miRNA microarray analysis. To evaluate the miRNA expression in lung tissue of rats after exposure of hexanal, Fischer-344 rats were inhaled to three concentrations (600, 1000, 1500 mg/m3) for 5 weeks. miRNA expression analysis was conducted using Rat miRNA 8 x 15K microarray v19.0 (Agilent Technologies, USA).
2014-08-08 | E-GEOD-60203 | biostudies-arrayexpress
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2014-08-08 | E-GEOD-60205 | biostudies-arrayexpress
Project description:With the population of older and overweight individuals on the rise in the Western world, there is an ever greater need to slow the aging processes and reduce the burden of age-associated chronic disease that would significantly improve the quality of human life and reduce economic costs. Caloric restriction (CR), is the most robust and reproducible intervention known to delay aging and to improve healthspan and lifespan across species (1); however, whether this intervention can extend lifespan in humans is still unknown. Here we report that rats and humans exhibit similar responses to long-term CR at both the physiological and molecular levels. CR induced broad phenotypic similarities in both species such as reduced body weight, reduced fat mass and increased the ratio of muscle to fat. Likewise, CR evoked similar species-independent responses in the transcriptional profiles of skeletal muscle. This common signature consisted of three key pathways typically associated with improved health and survival: IGF-1/insulin signaling, mitochondrial biogenesis and inflammation. To our knowledge, these are the first results to demonstrate that long-term CR induces a similar transcriptional profile in two very divergent species, suggesting that such similarities may also translate to lifespan-extending effects in humans as is known to occur in rodents. These findings provide insight into the shared molecular mechanisms elicited by CR and highlight promising pathways for therapeutic targets to combat age-related diseases and promote longevity in humans. Male Fisher 344 rats (n=54) were randomly assigned to two groups at 2 months of age. One group was kept ad libitum (AL) fed throughout their lifespan while the calorie restriction (CR) group was progressively brought down to a 40% CR. All animals were fed a NIH-31 standard chow (Harlan Teklad, Indianapolis, IN, USA). Rats were singly housed in an environmentally controlled vivarium with unlimited access to water and a controlled photoperiod (12 hr. light;12 hr. dark). Body weights and food intake were recorded biweekly. All rats were maintained between 68-72M-BM-0F according to animal protocols and NIH guidelines. Total RNA was extracted from the vastus lateralis skeletal muscle using Trizol Reagent (Invitrogen, Carlsbad, CA) following the manufacturerM-bM-^@M-^Ys instructions, n=5 from each group. Total RNA samples were biotin labeled and hybridized to RatRef-12 v1 Gene Expression beadchips (Illumina, San Diego, CA) following Illumina protocols. Arrays were washed and scanned using an Illumina BeadArray 500GX reader. Microarray florescent signals were extracted using the Illumina GenomeStudio Gene Expression software(v1.6.0) and any spots at or below the background were filtered using an Illumina detection p-value of 0.02 and above. The natural log of all remaining scores were used to find the avg and std of each array and the z-score normalization was calculated . Correlation analysis, sample clustering analysis and principal component analysis include all of probes are performed to identify/exclude any possible outliners. The resulting dataset was next analyzed with DIANE 6.0, a spreadsheet based microarray analysis program. Gene set enrichment analysis use gene expression values or gene expression change values for all of the genes in the microarray. Parametric analysis of gene set enrichment (PAGE) was used [pubmed 20682848] for gene set analysis. Gene Sets include the MSIG database [Link], Gene Ontology Database [Link], GAD human disease and mouse phenotype gene sets [pubmed: 20092628] were used to explore functional level changes.
2013-08-01 | E-GEOD-38062 | biostudies-arrayexpress
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2007-10-10 | E-GEOD-2852 | 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).
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Project description:The final goal of this study is to develop a short term and highly accurate prediction method of carcinogenicity based on gene expression profiles of rats subjected to carcinogen exposure. We conducted 3 day-, 14 day- and 28 day-repeated dose experiments in male F344 rats with 47 carcinogens and 26 non-carcinogens, and the gene expression profiles in liver were investigated by custom glass microarrays. Supplementary file "73 Compounds for training" indicates 47 carcinogens and 26 non-carcinogens. Supplementary file "15 Compounds for test" lists the other compounds which are for test. Two-condition experiment, control vs. chemical treated rat liver. Biological replicates: 4 control, 4 treated, control samples were pooled. One replicate per array.
2009-06-23 | E-GEOD-16743 | biostudies-arrayexpress
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2014-06-24 | E-GEOD-34136 | biostudies-arrayexpress
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