Acute Ozone-Induced Changes in Metabolic Processes and Liver Gene Expression: The Impact of Hepatic Vagotomy
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA661224 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The effects of ozone exposure were examined in rats that have undergone sham surgery or hepatic vagotomy
2021-04-01 | GSE157412 | GEO
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:Diet-induced circadian enhancer remodeling synchronizes opposing hepatic lipid metabolic processes
| PRJNA428990 | ENA
Project description:Ozone is a major air pollutant in highly populated areas. High levels of ambient ozone have been associated with decreased lung function and increased exacerbations of asthma in children and adults. However, the effects of ozone on the newborn’s lung are largely unknown. This study was aimed at profiling the newborn lung response to ozone at the transcriptome level to define the impact of ozone pollutant on the developing postnatal lung. Newborn mice were exposed to ozone or filtered normal air for 3 h. Total RNA was isolated from lung tissues at 6 and 24 h after completion of exposure and was subjected to gene expression analysis using Whole Mouse Genome Gene Expression 4X44K Microarrays (G2519F-014868, Agilent Technologies). Transcriptome analysis of the postnatal lung indicated that 455 genes were down-regulated and 166 genes were up-regulated by at least 1.5 fold at 6 h post-ozone exposure (t-test, p<0.05). At 24 h post exposure, 543 genes were down-regulated and 323 genes were up-regulated in the lungs of ozone-exposed newborn mice, compared to filtered air-exposed newborn mice (t-test, p<0.05). After controlling for false discovery rate, 50 genes were significantly down-regulated and only 4 genes were up-regulated at 24 h post ozone-exposure (q<0.05). Gene ontology enrichment analysis revealed that cell cycle-associated functions including cell division/proliferation, cellular assembly and organization were the predominant pathways negatively regulated by ozone exposure. These findings suggest that elevated ozone pollution may interfere with lung development and growth in the early age.
2014-03-12 | GSE45166 | GEO
Project description:Ozone is a major air pollutant in highly populated areas. High levels of ambient ozone have been associated with decreased lung function and increased exacerbations of asthma in children and adults. However, the effects of ozone on the newbornM-bM-^@M-^Ys lung are largely unknown. This study was aimed at profiling the newborn lung response to ozone at the transcriptome level to define the impact of ozone pollutant on the developing postnatal lung. Newborn mice were exposed to ozone or filtered normal air for 3 h. Total RNA was isolated from lung tissues at 6 and 24 h after completion of exposure and was subjected to gene expression analysis using Whole Mouse Genome Gene Expression 4X44K Microarrays (G2519F-014868, Agilent Technologies). Transcriptome analysis of the postnatal lung indicated that 455 genes were down-regulated and 166 genes were up-regulated by at least 1.5 fold at 6 h post-ozone exposure (t-test, p<0.05). At 24 h post exposure, 543 genes were down-regulated and 323 genes were up-regulated in the lungs of ozone-exposed newborn mice, compared to filtered air-exposed newborn mice (t-test, p<0.05). After controlling for false discovery rate, 50 genes were significantly down-regulated and only 4 genes were up-regulated at 24 h post ozone-exposure (q<0.05). Gene ontology enrichment analysis revealed that cell cycle-associated functions including cell division/proliferation, cellular assembly and organization were the predominant pathways negatively regulated by ozone exposure. These findings suggest that elevated ozone pollution may interfere with lung development and growth in the early age. Three-day old BALB/c mice were exposed for 3 h to ozone (1000 parts per billion). Age-matching littermate controls were exposed for 3 h to filtered normal air. Whole lung tissue was collected 6 and 24 h after completion of exposure to ozone or filtered air and was subjected to microarray analysis. Each time point was performed separately with its own filtered air littermate controls. Pups were cross-fostered during exposure so that all pups were with a dam during exposure. A total of 6-8 mice were initially included in each group and time point. Of these, n=4 mouse lungs were randomly selected for use in gene expression analysis.
2014-03-12 | E-GEOD-45166 | biostudies-arrayexpress
Project description:Overnutrition disrupts circadian rhythms leading to dysregulated metabolism by mechanisms that are not well understood. Here we show that diet-induced obesity (DIO) causes massive remodeling of circadian enhancer activity and gene transcription in mouse liver. Remarkably, DIO triggers synchronous, high amplitude circadian rhythms of both fatty acid (FA) synthesis and oxidation. This gain of circadian rhythmicity in lipid metabolic pathways that oppose each other emphasizes the importance of balance and flux in normal hepatic lipid metabolism. DIO-promoted rhythmicity of Sterol Regulatory Element-Binding Protein (SREBP) activation, which was required not only for the induction of FA synthesis but also, surprisingly, for FA oxidation (FAO). DIO also brought about a high amplitude circadian rhythm of peroxisome proliferated receptor a (PPARa), which was required for FAO. Provision of a pharmacological ligand for PPARa abrogated the requirement of SREBP for FA oxidation (but not FA synthesis), suggesting that SREBP indirectly controls FA oxidation via production of an endogenous PPARa ligand. Moreover, the high amplitude circadian rhythm of PPARa imparts time-of-day-dependent responsiveness to lipid-lowering drugs. Thus, acquisition of rhythmicity for the non-core clock components PPARa and SREBP1 remodels metabolic gene transcription in response to a challenging nutritive environment and enables a chronopharmacological approach to metabolic disorders.
2018-07-26 | GSE108878 | GEO
Project description:Ozone is a very common environmental pollutant and has been associated with the exacerbation of cardiopulmonary diseases like asthma. In this study the molecular mechanisms underlying the effect of ozone on airways hyperpermability were investigated. Two strains of mice, HeJ (Tlr4 mutant) and OuJ (wildtype) were exposed continuously to air or 0.3ppm of ozone. Lungs were removed and RNA was collected to generate expression profiles. Keywords: other
2003-07-16 | GSE476 | GEO
Project description:Populus deltoides and Populus trichocarpa were exposed to either ambient air or an acute ozone exposure of 200 ppb for 9 hrs and ozone response was profiled for each genotype by hybridising control against ozone-exposed samples per genotype. Keywords: stress response, genotype comparrison, ozone exposure
2009-04-01 | GSE10874 | GEO
Project description:In this study, integrated transcriptomics, proteomics and metabolomics approaches were applied to investigate the molecular responses of O3 in the leaves of two-weeks old rice (cv. Nipponbare) seedlings exposed to 0.2 ppm O3 for a period of 24 h. Based on the morphological alteration of O3-exposed rice leaves, transcript profiling of rice genes was performed in leaves exposed for 1, 12 and 24 h using rice DNA microarray chip, proteomics and metabolomics. This systematic survey showed that O3 triggers a chain reaction of altered gene, protein and metabolite expressions involved in multiple cellular processes in rice. Also investigated were the molecular responses in the leaves of two-weeks old rice (cv. Nipponbare) seedlings under continuous light and pure air (as a positive control for ozone exposure experiments) for a period of 24 h. Transcript profiling of rice genes was performed in leaves exposed for 1, 12 and 24 h using rice DNA microarray chip, proteomics and metabolomics. This systematic survey showed that continuous light and growth for 24 h also triggers a chain reaction of altered gene expressions involved in multiple cellular processes in rice, but different from those against ozone, in general. Keywords: Ozone fumigation response
2008-04-24 | GSE11157 | GEO
Project description:Ozone-modulated WRKY genes in Salvia officinalis: identification of up- and down-regulated genes upon acute ozone exposure
| PRJEB21536 | ENA