Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA122237 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We investigated morphometric structure and gene expression by microarray analysis in a small diameter artery, branch of the saphenous artery (a resistance artery), in representative models of renin-angiotensin system (RAS)-dependent and glucocorticoid hypertension, using the spontaneously hypertensive rat (SHR) and adrenocorticotropic hormone (ACTH)-induced hypertensive rat, respectively. Sixteen-week-old male Wistar-Kyoto (WKY) and age-matched spontaneously hypertensive rats (SHR) were used. Keywords: Comparison of global gene expression in resistance arteries of normotensive and genetically hypertensive rats and ACTH-treated rats.
2007-11-28 | GSE8051 | GEO
Project description:Genomic analysis of control and collateral arteries was used to investigate mechanisms responsible for impaired collateral growth in the Spontaneously Hypertensive rat, an animal model of essential hypertension with increased oxidative and nitrosative stress and metabolic abnormalities. A fundamental difference was observed in the overall expression pattern in SHR vs WKY collaterals. Redox related genes with altered expression included cyba (the gene encoding p22phox), superoxide dismutase 3, and thioredoxin reductases 1 and 2. Cystatin C, hevin, angiotensinogen, and the angiotensin type 1b receptor (AT1bR) had altered collateral expression that was confirmed by RT-PCR. These molecules are known to have significant roles in other types of arterial remodeling. Of specific interest was the AT1bR which exhibited up-regulation in WKY collaterals, but down-regulation in SHR. A remarkable increase in AT1R protein was observed in WKY but not SHR collaterals. Pharmacological blockade of the AT1R with losartan prevented collateral luminal expansion in WKY. In SHR, captopril restored redox status assessed by cyba expression and nitric oxide concentration, prevented collateral AT1bR down-regulation and re-established the capacity for collateral growth. These results indicate that redox-status significantly alters flow-mediated transcriptional regulation and demonstrate that increased flow-related expression/activation of the AT1R is required for normal collateral luminal expansion but is altered by chronic oxidative and/or nitrosative stress in hypertensive rats. Keywords: gene expression two strains: two vessel types
2010-12-15 | E-GEOD-19524 | biostudies-arrayexpress
Project description:We investigated morphometric structure and gene expression by microarray analysis in a small diameter artery, branch of the saphenous artery (a resistance artery), in representative models of renin-angiotensin system (RAS)-dependent and glucocorticoid hypertension, using the spontaneously hypertensive rat (SHR) and adrenocorticotropic hormone (ACTH)-induced hypertensive rat, respectively. Sixteen-week-old male Wistar-Kyoto (WKY) and age-matched spontaneously hypertensive rats (SHR) were used. Experiment Overall Design: There were 3 experimental groups: Group 1: 16-week male Wistar-Kyoto rats; Group 2: 16-week male Wistar-Kyoto rats treated with ACTH (0.1mg/kg/day) subcutaneously, for 4 weeks prior to sampling (i.e. during weeks 12-16 of life) ; Group3: 16-week male SHR (spontaneously hypertensive) rats. There were 3 replicate hybridizations in each experimental group. Due to the low yield of total RNA obtained from the arterial sections, each replicate was composed of RNA pooled from 2-3 different rats.
2008-06-15 | E-GEOD-8051 | biostudies-arrayexpress
Project description:Spontaneously Hypertensive Rat Genome
| PRJEB2025 | ENA
Project description:Analysis of global gene expression in mesenteric control and collateral arteries was used to investigate potential molecules, pathways and mechanisms responsible for impaired collateral growth in the Spontaneously Hypertensive rat (SHR). A fundamental difference was observed in the overall gene expression pattern in SHR vs. Wistar Kyoto (WKY) collaterals (only 6% of the genes altered in collaterals were similar). IPA analysis identified major differences between WKY and SHR in networks and biological functions related to cell growth and proliferation and gene expression. Canonical pathways identified by IPA in WKY but not SHR included nitric oxide and renin angiotensin system signaling. The angiotensin type 1 receptor (AT1R) exhibited up-regulation in WKY collaterals, but down-regulation in SHR; pharmacological blockade of the AT1R with losartan prevented collateral luminal expansion in WKY. In SHR control arteries, several mechano-sensitive and redox-dependent transcription regulators were down-regulated including Jun (-5.2X, P=0.02), Egr-1 (-4.1X, P=0.01), and NFkB1 (-1.95X, P=0.04). Predicted binding sites for NFkB and AP-1 were present in the genes altered in WKY but not SHR collaterals. Immunostaining demonstrated increased NFkB nuclear translocation in WKY but not SHR collaterals, and in collaterals of SHR treated with apocynin to restore a normal redox status. Based upon these results, we propose redox-dependent modulation of mechano-sensitive transcription factors as a mechanism to explain, at least in part, the fundamental differences in collateral gene expression between WKY and SHR and the impairment of collateral growth during chronic oxidative stress. Key words: arteriogenesis, microarray analysis, peripheral vascular disease, gene expression
2010-12-15 | GSE19524 | GEO
Project description:To investigate genetic basis of stroke susceptibility in an animal model of complex human disease, the stroke-prone spontaneously hypertensive rat (SHRSP).
2016-06-26 | E-MTAB-3688 | biostudies-arrayexpress
Project description:In order to investigate the molecular basis of carotid body chemoreceptor sensitisation in the Spontaneously Hypertensive Rat (SHR) we have sequenced the transcriptomes of bilateral carotid body samples from aged-matched, male SHR and control Wistar-Kyoto rats.
2022-01-11 | GSE178504 | GEO
Project description:Small artery remodeling depends on the genetic background in spontaneously hypertensive rats (microRNA)
| PRJNA231845 | ENA
Project description:Small artery remodeling depends on the genetic background in spontaneously hypertensive rats (mRNA)
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Project description:Transition from Compensated Hypertrophy to Systolic Heart Failure in the Spontaneously Hypertensive Rat
| PRJNA120823 | ENA