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ABSTRACT:
PROVIDER: PRJNA231842 | ENA |
REPOSITORIES: ENA
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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)
| PRJNA231846 | ENA
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: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:The goals of the study are to compare differently expressed genes in heart tissues of hypertensive rats (spontaneously Hypertension Rats, SHR) with age-matched control rats (wistar Rats, WKY), identify new targets to reverse hypertension induced cardiac remodeling and idetify the targets of Traditional Chinese Medicine QDG.
2020-01-31 | GSE144548 | GEO
Project description:Spontaneously hypertensive rats (SHR) have been used frequently as a model for human essential hypertension. However, both the SHR and its normotensive control, the Wistar Kyoto rat (WKY), consist of genetically different sublines. We tested the hypothesis that discrepant data in literature regarding the pathophysiology of vascular remodeling in hypertension result from the use of different rat sublines. Using micro-arrays, we studied miRNA and mRNA expression in resistance arteries of WKY and SHR from three different sources, at 6 weeks and 5 months of age. Both WKY and SHR showed an age-related expression pattern that involved many genes related to the extracellular matrix. In SHR, this pattern was more extensive and included a specific increase in miR132-3p, and type III deiodinase. Direct comparison of WKY to SHR also yielded differences in expression, including thrombospondin 4. Heterogeneity in gene expression among sublines was associated with differences in blood pressure, body weight, vascular remodeling, endothelial function, and vessel ultrastructure. Common features in vessels from SHR were an increase in wall thickness, wall-to-lumen ratio, and internal elastic lamina thickness. These results indicate that endothelial dysfunction, vascular stiffening, and inward remodeling of small arteries are not common features of hypertension, but are subline-dependent. Relatively minor differences in genetic background associate with different types of vascular remodeling in hypertensive rats. The clinical implication of this study is that more research into personalized treatment in hypertension is warranted.
2015-10-02 | GSE53361 | GEO
Project description:Spontaneously hypertensive rats (SHR) have been used frequently as a model for human essential hypertension. However, both the SHR and its normotensive control, the Wistar Kyoto rat (WKY), consist of genetically different sublines. We tested the hypothesis that discrepant data in literature regarding the pathophysiology of vascular remodeling in hypertension result from the use of different rat sublines. Using micro-arrays, we studied miRNA and mRNA expression in resistance arteries of WKY and SHR from three different sources, at 6 weeks and 5 months of age. Both WKY and SHR showed an age-related expression pattern that involved many genes related to the extracellular matrix. In SHR, this pattern was more extensive and included a specific increase in miR132-3p, and type III deiodinase. Direct comparison of WKY to SHR also yielded differences in expression, including thrombospondin 4. Heterogeneity in gene expression among sublines was associated with differences in blood pressure, body weight, vascular remodeling, endothelial function, and vessel ultrastructure. Common features in vessels from SHR were an increase in wall thickness, wall-to-lumen ratio, and internal elastic lamina thickness. These results indicate that endothelial dysfunction, vascular stiffening, and inward remodeling of small arteries are not common features of hypertension, but are subline-dependent. Relatively minor differences in genetic background associate with different types of vascular remodeling in hypertensive rats. The clinical implication of this study is that more research into personalized treatment in hypertension is warranted.
2015-10-02 | GSE53363 | GEO
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.
2024-02-27 | PXD048882 | Pride
Project description:This study aimed at integrating metabolomics and proteomics data for a comprehensive view of the molecular targets of intervention of protein extracts from Tenebrio molitor in treating hypertension. Serum samples from spontaneously hypertensive rats and Wistar Kyoto rats were analyzed using a quantitative metabolomics and label-free proteomics approach based on liquid chromatography coupled with high resolution mass spectrometry (LC-HRMS). Among deregulated metabolites and proteins in hypertensive rats, we found 15 metabolites and 17 proteins that were restored by supplementation with Tenebrio molitor protein extract. The combination of metabolomics and proteomics provided useful data to uncover the molecular targets of intervention and the underlying functional mechanism of Tenebrio molitor protein extract in an animal model such as spontaneously hypertensive rats. The results suggested that Tenebrio molitor supplementation could effectively treat hypertension, partially by regulating proteins and molecules mainly involved in biological pathways associated to angiotensinogen-angiotensin, Serin protease inhibitors, kallikrein–kinin, reactive oxygen scavenging, and lipid peroxidation.
2022-10-13 | PXD034456 | Pride
Project description:Abstract Background: Long-term hypertension can lead to hypertensive heart disease, which ultimately progresses to heart failure. As an angiotensin receptor blocker (ARB) antihypertensive drug, allisartan can control blood pressure and improve cardiac remodeling and cardiac dysfunction caused by hypertension. The objective of this study is to investigate the protective effects of Allisartan on the heart of spontaneously hypertensive rats (SHRs) and the underlying mechanisms. Methods: We used spontaneously hypertensive rats (SHRs) as an animal model of hypertensive heart disease and treated them with allisartan orally at a dose of 25 mg/(Kg·day). We continuously monitored the rats' blood pressure levels, measured their body and heart weights, and evaluated their cardiac structure and function using echocardiography. WGA staining and Masson trichrome staining were employed to assess the morphology of the myocardial tissue. We performed transcriptome and proteome analysis using the Solexa/Illumina sequencing platform and tandem mass tag (TMT) technology, respectively. We used immunofluorescence co-localization to analyze Nrf2 nuclear translocation, and TUNEL to detect the level of cell apoptosis. The protein and mRNA levels were determined by Western blotting and qRT-PCR, respectively. Results: Allisartan lowered blood pressure, attenuated cardiac remodeling, and improved cardiac function. Allisartan alleviated cardiomyocyte hypertrophy and cardiac fibrosis. Allisartan significantly affected the pentose phosphate pathway, fatty acid elongation, valine, leucine and isoleucine degradation, glutathione metabolism, and amino sugar and nucleotide sugar metabolism pathways in the hearts of SHRs, and upregulated the expression level of GSTM2. Allisartan activated the PI3K-AKT-Nrf2 signaling pathway and inhibited cardiomyocyte apoptosis. Conclusions: Our study determined that allisartan effectively controls blood pressure in SHRs and improves cardiac remodeling and cardiac dysfunction. Allisartan upregulates the expression level of GSTM2 in the hearts of SHRs and significantly affects glutathione metabolism shown by transcriptomics and proteomics analysis. The cardioprotective effect of allisartan may be mediated through activation of the PI3K-AKT-Nrf2 signaling pathway, upregulation of GSTM2 expression, and reduction of SHRs cardiomyocyte apoptosis.
2024-02-27 | GSE254800 | GEO