Project description:We used spontaneously hypertensive rats (SHRs) as an animal model of hypertensive heart disease and treated them with allisartan orally. We continuously monitored the rats' blood pressure levels, measured their body and heart weights, and evaluated their cardiac structure and function using echocardiography. We performed proteome analysis using the tandem mass tag (TMT) technology.
Project description:Spontaneously hypertensive rat (SHR; Rat Genome Database (RGD) ID: 631848) is probably the most commonly used rodent model for essential hypertension. Its minimal congenic subline PD5 ( SHR.PD-(D8Rat42-D8Arb23)/Cub; (RGD ID: 1641851)) which differs by a short segment of chromosome 8 (encompassing only 7 genes) displays lower levels of blood pressure and amelioration of cardiac fibrosis compared to SHR. We used microarray aproach to unravel gene expression differences between SHR and PD5 responsible for the different phenotypes in our rat strains.
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.
Project description:Primary outcome(s): Analysis of the diversity and composition of the gut microbiome by 16S rRNA sequencing
Study Design: Observational Study Model : Others, Time Perspective : Prospective, Enrollment : 60, Biospecimen Retention : Collect & Archive- Sample with DNA, Biospecimen Description : Blood, Stool
Project description:Examination of gene expression associated with hypoxia treatment of parental Fawn Hooded Hypertensive (FHH) and consomic Brown Norway (FHH1BN) rat strain. FHH1BN rats are derived from introgression of chromosome 1 from BN rats into the FHH genetic background.
Project description:To determine if there exists a consistent gene signature associated with vascular hypertrophy among different rat hypertensive models: treated and untreated Wistar Kyoto (WKY) rats and treated and untreated Spontaneous Hypertensive Rat (SHR) rats. Keywords: strain comparison, treatment vs control