Ozone exposure differentially changed global gene expression at brainstem and hypothalamus in healthy (SHAM) and adrenalectomized rats
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PROVIDER: PRJNA551004 | ENA |
REPOSITORIES: ENA
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Project description:Ozone exposure in SHAM rats resulted in increases and decreases in expression of hundreds of genes in brainstem and hypothalamus relative to air-exposed SHAM rats (303 and 568 genes, respectively). Adrenalectomy in air-exposed rats resulted in few significant transcriptional differences in the brainstem and hypothalamus (~20 genes per tissue). Differentially expressed genes from ozone exposure were enriched for pathways involving hedgehog signaling, responses to alpha-interferon, hypoxia, and mTORC1, among others. Gene changes in both brain areas were analogous to those altered by corticosteroids and L-dopa, suggesting a role for endogenous glucocorticoids and catecholamines. AD completely prevented this ozone-induced transcriptional response. These findings show that short-term ozone inhalation promotes a shift in brainstem and hypothalamic gene expression that is dependent on the presence of circulating adrenal-derived stress hormones.
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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.
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Project description:The effects of ozone exposure were examined in rats that have undergone sham surgery or hepatic vagotomy
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Project description:Air pollutant exposures have been linked to systemic disease; however, underlying mechanisms between single-tissue exposures and systemic responses are poorly understood. A prototypic inducer of stress, ozone causes respiratory and systemic, multiorgan effects through neuroendocrine stress response activation. The goal of the presented study was to assess transcriptomic signatures of multiple tissues and serum metabolomics to understand how neuroendocrine and adrenal-derived stress hormones contribute to multiorgan health outcomes. Male Wistar Kyoto rats (12-13 weeks old) were exposed to filtered air or 0.8 ppm ozone for 4-hours, and blood/tissues were collected immediately post-exposure. Each tissue had distinct expression profile at baseline. Ozone changed (adjusted p-value < .1, absolute fold-change > 50%) 5,102 genes in muscle, 2,516 in adrenals, 1,640 in lung, 1,333 in liver, 1,242 in adrenals and 274 in hypothalamus. Serum metabolomic analysis identified 863 metabolites, of which 447 were significantly altered in ozone-exposed rats (adjusted p-value < .1, absolute fold change > 20%). Although overall hypoxia, GPCR signaling and glucocorticoid signaling pathways were commonly changed in most tissues, gene signatures within overrepresented pathways showed limited overlap between tissues. This pattern suggested the distribution of receptors and transcriptional mechanisms for stress hormones are likely tissue-specific and involve induction of different gene sets with shared initiating triggers. Metabolomic analysis suggested major changes in lipids, amino acids and metabolites linked to gut microbiome, which correlated with transcriptional changes identified through pathway analysis within liver, muscle, and adipose tissues. Systems-level examination of tissue-specific biological mechanisms could further understanding of air pollution-related health consequences.
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