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.
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
Project description:Ozone is known to induce gene expression in plants. The roles of the induced genes and the molecular basis for the induction however largely remain to be elucidated. We will expose 2 week-old Arabidopsis seedlings to 200 ppb ozone for 1 h. RNA will be extracted from control and ozone-fumigated seedlings 3 h following the end of the fumigation period. The induction of the known anti-oxidant enzyme GST will be confirmed prior to submission of the RNA samples to GARNet. Changes in gene expression will be assessed by hybridising microarrays with fluorescently labelled cDNA prepared from control and ozone-fumigated seedlings. The role of selected genes will be inferred from their sequence and further established by over expression under the control of the 35S or cell-specific promoters and by searching for mutants among single transposon or T-DNA insertion collections. Plants will be analysed on the basis of traits that are known to be affected by ozone including growth, flowering and stomatal responses. In addition, the ozone calcium signature we have reported previously (Clayton et al.1999) will be studied by crossing transgenic or mutant plants with apoaequorin or yellow cameleon 2.1-transformed plants. Experimenter name = Eleri Short Experimenter phone = 01524 593929 Experimenter fax = 01524 843854 Experimenter department = Department of Biological Sciences Experimenter institute = Lancaster University Experimenter address = Department of Biological Sciences Experimenter address = Lancaster University Experimenter address = Lancaster Experimenter zip/postal_code = LA1 4YQ Experimenter country = UK Keywords: compound_treatment_design
Project description:Ozone, the major component of air pollution, is an oxidant gas. Inhalation of high ambient levels of ozone causes oxidative stress and airway inflammation. To assess the biological responses of airway inflammatory cells to ozone-induced oxidative stress, we examined the gene expression of airway inflammatory cells in response to inhalation of ozone.