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Whole genome analysis of nicotine-exposed cells from the brainstem of spontaneously hypertensive and Wistar Kyoto rats

ABSTRACT: The development of hypertension may be highly influenced by the use of nicotine especially in genetically susceptible subjects. In this study the effects of nicotine on gene expression of cultured cells from the brainstem of spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats were evaluated using whole genome microarray platforms. It was described for the first time that nicotine may act differentially on the gene expression profile of SHR and WKY. The influence of strain was present in 348 genes that were differentially expressed in SHR as compared to WKY brainstem cells independently of the nicotine treatment. 176 genes had their expression altered in both strains after nicotine exposure. Interaction between nicotine treatment and the strain was observed for the expression of 269 genes which participate of cellular pathways related to neurotrabnsmitter secretion, intracellular trafficking and cell communication. In conclusion, this study leaves a list of genes whose expression shall be better studied since they are good candidates to the phenotypic differentiation between SHR and WKY, including hypertension as well as demonstrated that alterations in the systems of intracellular trafficking and neurotransmission may be relevant to the development of hypertension.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE13311 | GEO | 2009/09/16

SECONDARY ACCESSION(S): PRJNA109895

REPOSITORIES: GEO

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Project description:DEP exposure is linked to increases in cardiovascular effects. This effect is enhanced in individuals with pre-existing disease. Animal models of cardiovascular disease are used to study this susceptibility. The heart is rich in mitochondria, which produce high levels of free radicals, leading to inactivation of tricarboxylic acid cycle enzymes. We hypothesized that a 4-wk DEP inhalation would result in strain-related structural impairment of cardiac mitochondria and changes in these enzyme activities in WKY and SHR. Male rats (12-14 wks age) were exposed whole body to air or 0.5 or 2.0 mg/m3 DEP for 6h/d, 5 d/wk for 4 wks. Neutrophilic influx was noted in the bronchoalveolar lavage fluid in both strains. A slightly lower level of baseline cardiac mitochondrial aconitase activity was seen in SHR than WKY. Aconitase activity appeared to be decreased in an exposure related manner in both strains. Significantly higher baseline levels of cardiac cytosolic ferritin and aconitase activity were seen in the SHR than WKY. No exposure-related changes were noted in either of these measures. Mitochondrial succinate and isocitrate dehydrogenase activities were not changed following DEP exposure in either strain. Transmission electron microscopy images of the heart indicated abnormalities in cardiac mitochondria of control SHR but not control WKY. No exposure related ultrastructural changes were induced by DEP in either strain. In conclusion, strain differences in cardiac biomarkers of oxidative stress and structure of mitochondria exist between SHR and WKY. DEP exposure results in small changes in cardiac mitochondrial and cytosolic markers of oxidative stress. (Abstract does not represent USEPA policy.) Experiment Overall Design: Two strains of rats (Wistar Kyoto (WKY) and spontaneously hypertensive (SH) rats were exposed to either diesel exhaust particles or clean air. Four biological replicates were used for each strain/treatment exposure. Total number of chips equals 16.

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Whole genome analysis of nicotine-exposed cells from the brainstem of spontaneously hypertensive and Wistar Kyoto rats

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