Rattus norvegicus strain:Wistar-Kyoto
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA344754 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Wistar Kyoto rat stellate ganglia transcriptome
| PRJNA505849 | ENA
Project description:We measured gene expression in the adrenal glands of the Spontaneously Hypertensive Rat (SHR) and Wistar-Kyoto rat (WKY) using Affymetrix RG-U34A GeneChips. All rats were aged-matched at 4-weeks. The rats were obtained from the colonies at the Univeristy of California San Diego, La Jolla, CA.
2007-11-01 | E-GEOD-1675 | biostudies-arrayexpress
Project description:Hypertension is a multifactor disease that possibly involves alterations in gene expression in hypertensive relative to normotensive subjects that are largely unknown. In this study we used high-density oligoarrays to compare gene expression profiles in cultured neurons and glia from pons and medulla oblongata of newborn spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats, a widely documented animal model of hypertension. We found 358 genes differentially expressed between SHR and WKY brainstem cells that preferentially map to 24 metabolic/signaling pathways. Some of the pathways and regulated genes identified herein are obviously related to blood pressure regulation; however there are several genes differentially expressed in SHR not yet associated to hypertension or participating in blood pressure regulation. These constitute a rich resource for the identification and characterization of novel genes involved in hypertension development, or associated to phenotypical differences observed in SHR relative to WKI. In conclusion, this study describes for the first time the gene profiling pattern of brainstem cells from SHR and WKY rats, which opens up new possibilities and strategies of investigation and possible therapeutics to hypertension, as well as for the understanding of the brain contribution in this pathology. Keywords: Gene expression profiling of cultured cells from brainstem of spontaneously hypertensive and normotensive Wistar Kyoto rats
2008-12-31 | GSE10366 | GEO
Project description:Nephrotoxic nephritis induction in inbred rat strains (Wistar Kyoto and Lewis) and transcription profiling
2008-04-01 | E-MEXP-1294 | biostudies-arrayexpress
Project description:Left ventricular gene expression profiles from 12-, 16- and 20-months old spontaneously hypertensive rats (SHRs) were compared with left ventricular profiles seen in age-matched Wistar-Kyoto (WKY) rats [control rats] by screening Affymetrix U34A arrays (there are 4 samples in each timepoint except 3 samples of 20-months old WKYs).
2007-09-20 | E-GEOD-2116 | biostudies-arrayexpress
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.
2008-10-20 | E-GEOD-9694 | biostudies-arrayexpress
Project description:Although fatty liver disease is caused by a number of toxicological insults and the metabolic syndrome, the exact mechanisms by which many of these pathophysiological stimulii induce fatty liver are unknown. The rapid and profound steatosis caused by orotic acid, resulting from an impairment in the production of ApoB, has been investigated in the Wistar strain rat using a combined transcriptomic and metabonomic/metabolomic approach. Analysis of liver tissue from rats exposed to orotic acid for 1, 3, and 14 days was performed by DNA microarrays and high resolution 1H NMR spectroscopy based metabonomics of both tissue extracts and intact tissue (n = 3). Data were analyzed using a combination of ANOVA and principal components analysis, used as a data reduction tool to visualize the most perturbed transcripts and metabolites. Orotic acid produced a profound 8-fold increase in total lipids, and in particular increases in resonances associated with polyunsaturated fats (CHCH and CH2CHCH groups). This was accompanied by increases in the concentrations of trimethylamine-oxide (TMAO), betaine, choline, and phosphocholine, as well as a relative decrease in glucose and glycogen. At the transcriptional level, perturbations were detected in both oxidative stress and osmoregulation/pH homeostasis. However, this contrasts with a previous transcriptomic/metabolic study of fatty liver disease in a combined data set of Wistar (out-bred) and Kyoto (in-bred) strains of rats, with only 4 transcripts being found to be in common between the two analyses. This emphasizes the need to understand how strain background interacts with a given toxic lesion or genetic modification. Keywords: metabolomics . metabolic profiling . pattern recognition . nonalcoholic steatohepatisis
2009-03-11 | E-BIID-1 | biostudies-arrayexpress
Project description:A time course of orotic acid induced fatty liver disease. Kyoto and Wistar strain rats were exposed to orotic acid for days 1, 3 and 14. Controls are also included. Keywords = Wistar Keywords = Kyoto Keywords = orotic acid Keywords: time-course
2004-09-16 | GSE665 | GEO
Project description:Acute acrolein inhalation in male rats resulted in multi-tissue transcriptomic alterations that were observed through Illumina mRNA sequencing. Specifically, site-specific respiratory expression profile differences were noted between air- and acrolein-exposed groups. Nasal epithelial tissue demonstrated 452 differentially expressed genes (DEGs) (310 up-regulated and 142 down-regulated)and lung tissue demonstrated 95 DEGs (80 up-regulated and 15 down-regulated). Notable transcriptomic alterations were also observed in liver tissue of acrolein-exposed rats, with 1699 identified DEGs (788 up-regulated and 911 down-regulated). A variety of mRNA expression profile differences resulting from acute acrolein inhalation was observed in other peripheral tissues, including adipose, muscle, adrenals, hippocamus, and hypothalamus. Gene changes were largely representative of oxidative and inflammatory response in the nose, as well as xenobiotic metabolism changes in the lung. Liver changes, which were most numerous, included alterated metabolic signaling (Sirtuin and FXR signaling), as well as alterated oxidoreductive, GPCR, and glucocorticoid pathways. Together, these data demonstrate acrolein, a well-characterized respiratory irritant, induces systemic neuroendocrine immunological and metabolic stress.
2023-11-16 | GSE247698 | GEO