Next Generation Sequencing Quantitative Analysis of PCB-exposed and Sham-exposed Rats Liver, Brain, Thymus and Spleen Transcriptomes
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE179117 | GEO | 2021/06/30
REPOSITORIES: GEO
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Project description:Polychlorinated biphenyls (PCBs) are persistent environmental toxicants that pose a variety of health risks in humans. PCB 52 has been found in the indoor air of schools where adolescent students and staff are being actively exposed. This study examined the livers of adolescent Sprague-Dawley rats after sub-acute exposure to PCB 52 via nose-only inhalation. Rats were exposed for 4 hours daily for 28 consecutive days. RNA extracted from both male and female livers were submitted for RNA sequencing to compare the effects of PCB 52 on the expression of genes in the liver.
2024-02-27 | GSE255048 | GEO
Project description:Polychlorinated biphenyls (PCBs) are persistent environmental toxicants that pose a variety of health risks in humans. PCB 52 has been found in the indoor air of schools where adolescent students and staff are being actively exposed. This study examined the three different fat depots, namely, brown adipose tissue (BAT), subcutaneous adipose tissue (SAT), and visceral adipose tissue (VAT), of adolescent Sprague-Dawley rats after sub-acute exposure to PCB 52 via nose-only inhalation. Rats were exposed for 4 hours daily for 28 consecutive days. RNA extracted from both male and female fat depots were submitted for RNA sequencing to compare the effects of PCB 52 on the expression of genes in the fat depots.
2024-03-04 | GSE259369 | GEO
Project description:The present research aimed to investigate peripheral blood gene expression profiling as a minimally invasive surrogate approach to study silica-induced pulmonary toxicity. Rats were exposed to crystalline silica by inhalation (15 mg/m3, 6 hours/day, 5 days). Pulmonary damage and blood gene expression profiles were determined at various latency periods (0 - 16 weeks). Silica exposure resulted in pulmonary toxicity and this was evidenced by histological changes in the lungs and elevation of LDH activity, and total protein and albumin contents in the bronchoalveolar lavage fluid (BALF) of the rats. Microarray analysis of global gene expression profiles in the blood of the rats identified genes that were differentially expressed in response to silica exposure and toxicity. The number of significantly differentially expressed genes in the blood of silica exposed rats correlated with the severity of silica-induced pulmonary toxicity. Genes involved in biological functions such as inflammatory response, cancer, pulmonary damage, oxidative stress, energy metabolism, fibrosis, etc, were found differentially expressed in the blood of the silica exposed rats compared with the controls. Induction of pulmonary inflammation in the silica exposed rats, as suggested by differential expression of inflammatory response genes in the blood, was supported by significant increases in the number of macrophages and infiltrating neutrophils as well as the activity of pro-inflammatory chemokines M-bM-^@M-^S MCP1 and MIP2, observed in the BALF of the silica exposed rats. A silica-responsive blood gene expression signature developed using the gene expression data predicted with significant accuracy the exposure of rats to lower concentrations (1 and 2 mg/m3) of silica. Taken together our findings suggest the potential application of peripheral blood gene expression profiling as a minimally invasive and efficient surrogate approach to detect and study silica-induced pulmonary toxicity. 96 samples were analyzed in this experiment. The RNA from rat blood samples was isolated for gene expression studies. Rats (48) were exposed to crystalline silica by inhalation (15 mg/m3, 6 hours/day, 5 days) and air (24). Blood gene expression profiling was performed using rat blood samples, 8 each for silica exposed and 4 each for air exposed controls at various post-exposure time periods (0, 1, 2, 4, 8, and 16 weeks). A silica-responsive blood gene expression signature was developed using the gene expression data obtained from the 0 week post-exposure group and the control rats. The signature was tested for predicting silica exposure and resulting toxicity in the rats exposed to lower concentrations (1 and 2 mg/m3) of silica (8 rats per group) and air (8 rats).
2011-12-02 | E-GEOD-27023 | biostudies-arrayexpress
Project description:Ozone-induced lung injury/inflammation and pulmonary/hypothalamus gene expression are diminished in adrenalectomized (ADREX) rats. Acute ozone exposure induces metabolic alterations concomitant with increases in epinephrine and corticosterone. We hypothesized that adrenal hormones are responsible for observed hepatic ozone effects, and in ADREX rats, these changes would be diminished. Five-seven days after sham or ADREX surgeries, male Wistar-Kyoto rats were exposed to air or 0.8-ppm ozone for 4-hrs. Serum samples were analyzed for metabolites and liver for transcriptional changes immediately post-exposure. Ozone increased circulating triglycerides, cholesterol, free fatty acids, and leptin in sham but not ADREX rats. Ozone-induced inhibition of glucose-mediated insulin release was reversed in ADREX rats. Unlike diminution of hypothalamus and lung mRNA expression changes, ADREX in air-exposed rats (ADREX-air/sham-air) caused differential expression of ~1000 genes in liver. Likewise, ~1000 genes were differentially expressed in ozone-exposed ADREX rats (ADREX-ozone/ADREX-air). Ozone-induced hepatic changes in sham rats reflected enrichment for pathways involving metabolic processes, including acetyl-CoA biosynthesis, TCA cycle, and sirtuins. Upstream predictor analysis identified significant similarity to glucocorticoids and pathways involving CREBBP. These changes were absent in ADREX rats exposed to ozone. However, ozone caused unique changes in ADREX liver mRNA reflecting activation of synaptogenesis, neurovascular coupling, neuroinflammation, and insulin signaling with inhibition of senescence pathways. In these rats, upstream predictor analysis identified numerous microRNAs involved under glucocorticoid insufficiency. These data demonstrate the critical role of adrenal stress hormones in ozone-induced hepatic homeostasis and the need for further research elucidating their role in propagating environmentally driven diseases.
2022-11-02 | GSE196818 | GEO
Project description:Synergism of Iraqi Sand/Cigarette Smoke Co-Exposure in Rats. 24 samples are used. A total of 102 rats will be separated into six exposure groups: each group consisting of 17 male CD Sprague-Dawley rats, 10 to 15 weeks old. The six exposure groups were each exposed via two routes: 1. nose-only inhalation exposures --- air or cigarette smoke; 2. whole-body inhalation exposures -- air or manufactured silica sand or Iraqi sand. The nose only exposures were conducted 3 hours per day, 5 days per week for 6 weeks. During the last two weeks of the nose - only exposures, whole-body exposure were also conducted 18-19 hours per day, 7 days per week.
2012-01-01 | E-GEOD-28804 | biostudies-arrayexpress
Project description:Exposure to indoor air pollution generated from the combustion of solid fuels is a major risk factor for a spectrum of cardiovascular and respiratory diseases, including lung cancer. In Chinaâs rural counties of Xuanwei and Fuyuan, lung cancer rates are among the highest in the country. While the elevated disease risk in this population has been linked to the widespread usage of bituminous (smoky) coal as compared to anthracite (smokeless) coal, the underlying physiologic mechanism that smoky coal induces in comparison to other fuel types is unclear. As we have previously used airway gene-expression profiling to gain molecular insights into the physiologic effects of cigarette smoke, here we profiled the buccal epithelium of residents exposed to the burning of smoky and smokeless coal in order to understand the physiologic effects of solid fuels. Buccal mucosa scrapings were collected from healthy, non-smoking female residents of Xuanwei and Fuyuan counties who burn coal indoors. RNA was isolated and hybridized onto Affymetrix Human gene 1.0 ST GeneChips, capturing the gene-expression response of (n=26) smoky coal users and (n=9) smokeless coal users. 24-hour indoor personal exposure levels (PM2.5, Polycyclic Aromatic Hydrocarbons) were also captured during this sampling period.
2015-11-02 | E-GEOD-64277 | biostudies-arrayexpress
Project description:Printer emitted particles (PEPs)-induced cardiopulmonary adverse effects and health risks and the underlying mechanisms are unknown. The aim of this study was to perform genome-wide mRNA profiling in rat blood to identify non-invasive blood based biomarkers for medical and occupational surveillance. The rats were exposed to printer emitted particles PEPs (exposed) and high efficiency particulate air (HEPA) filtered air (control). Animals were sacrificed on 1, 5, 9, and 21 days for lung tissue collection.
2020-01-13 | GSE127950 | GEO