RNAseq of perivascular adipose tissue from mesenteric arteries from normotensive and hypertensive Dahl S rats
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA694168 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We report the results from RNA-seq analysis of perivascular adipose tissues (PVAT) collected from mesenteric arteries from Dahl S rats. Animals were on a control or a high fat diet for 24 weeks. At the moment of collection, rats fed high fat diet were hypertensive. In contrast, rats on the control diet were normotensive.
2021-01-23 | GSE165369 | GEO
Project description:The dynamic nature of the microtubule network is regulated in part by post-translational modifications – particularly through acetylation, which stabilizes the microtubule network. Whether post-translational modifications of the microtubule network in vascular smooth muscle cells contribute to the pathophysiology of hypertension is unknown. The aim of this study was to determine the acetylated state of the microtubule network in the mesenteric arteries of spontaneously hypertensive rats (SHR), and investigate whether sustained acetylation via treatment with a histone deacetlyase-6 (HDAC-6) inhibitor, tubacin, would affect isoprenaline-mediated vasorelaxations in normotensive and hypertensive vessels.Using Western blotting, and mass spectrometry, we show that acetylation of the microtubule network is increased in the mesenteric arteries of the SHR compared to normotensive rats. Using wire myography, we found that tubacin enhanced the β-adrenoceptor-mediated vasodilatation by isoprenaline when the endothelium was intact, but attenuated relaxations when the endothelium was denuded or nitric oxide production was inhibited. By pre-treating vessels with colchicine to disrupt the microtubule network, we were able to confirm that the effects of tubacin were microtubule-dependent. Using SICM, we examined the cell surface Young’s Modulus of smooth muscle cells, but found no difference between control, tubacin-treated, or taxol-treated cells.Acetylation of the microtubule network is elevated in mesenteric arteries from the SHR. Furthermore, this study shows that tubacin has an endothelial-dependent bimodal effect on isoprenaline-mediated vasorelaxation. These findings pave the way for evaluation of HDAC inhibitors in the treatment of hypertension in human clinical studies.
2024-02-21 | PXD045602 | Pride
Project description:The Dahl salt-sensitive (S) rat model develops chronic hypertensive disease when fed a high salt diet that ultimately results in renal and heart failure, as well as prevalent cerebrovascular pathologies. Phenotypic changes in the cerebral vasculature are preceded by changes in gene expression, and evidence supports a role for extracellular signal-regulated kinase 1/2 (ERK1/2) in vascular cell proliferation, yet little is known regarding ERK1/2 –regulated gene transcription in cerebrovascular smooth muscle during hypertension. Findings presented here support the hypothesis that salt-induced hypertensive disease results in upregulation of ERK1/2 activity and ERK1/2-regulated genes that promote remodeling in cerebral resistance arteries. Dahl S rats were fed either a 0.4% NaCl (low salt, LS) or 8% NaCl (high salt, HS) diet until evidence of left ventricular dysfunction. Gene expression profiling using oligonucleotide array analysis detected a significant fold-change of 1.5 or greater in 133 out of 15,923 genes examined. Mitogen-activated protein kinase (MAPK)-regulated genes were overrepresented and provided a link to genes involved in proliferation and extracellular matrix signaling including plasminogen activator inhibitor I (PAI-1), osteopontin (OPN) and junB. These data suggests that salt induced hypertensive disease promotes hyperplasia and changes in matricellular genes that are likely important in vascular remodeling. Keywords: Normotensive vs. Hypertensive Disease
2007-08-09 | GSE5488 | GEO
Project description:We examined gene expression profiles in the rat mesenteric arteries using genome-wide microarray technology, and determined gene expression profiles in 3 rat strains and treated ones: spontaneously hypertensive rats (SHR), stroke-prone SHR (SHRSP), and normotensive WKYs treated with 2K1C or 1K1C, or without operation for 3 weeks at 6 weeks of age. To identify candidate genes involved in the genesis of hypertension in the SHR strains in comparison to renal hypertensive WKY, we compared the gene expression levels at 6 weeks of age, isolated genes showing a more than 4-fold increase or a less than 1/4-fold compared with WKY treated with 2K1C, 1K1C or none.
2019-03-19 | GSE74288 | GEO
Project description:Using data-independent acquisition-based mass spectrometry analysis, we determined the protein changes in cerebral arteries in pre- and early-onset hypertension from the spontaneously hypertensive rat (SHR), a model that resembles essential hypertension. Our analysis identified 125 proteins with expression levels that were significantly up- or downregulated in 12-week old SHRs compared to normotensive Wistar Kyoto rats. Using an angiogenesis enrichment analysis, we identified a critical imbalance in angiogenic proteins, promoting an anti-angiogenic profile in cerebral arteries at the early-onset of hypertension. In a comparison to previously published data, we demonstrate that this angiogenic imbalance is not present in mesenteric and renal arteries from age-matched SHRs. Finally, we identified two proteins (Fbln5 and Cdh13), whose expression levels were critically altered in cerebral arteries compared to the other arterial beds. The observation of an angiogenic imbalance in cerebral arteries from the SHR reveals critical protein changes in the cerebrovasculature at the early-onset of hypertension and provides novel insight into the early pathology of cerebrovascular disease.
2023-09-20 | PXD040818 | Pride
Project description:Vascular smooth muscle cells require beta1 integrin for survival. Following the induced deletion of smooth muscle beta1 integrin, smooth muscle cells undergo apoptosis and arteries become fibrotic. This microarray study on mesenteric arteries 2 weeks after the initiation of beta1 integrin deletion specifically in smooth muscle cells of the adult mouse aimed to examine early changes in expression following deletion. Mesenteric arteries from three wild type mixed background and three beta1 integrin smooth muscle knockout mixed background mice are examined.
2013-02-26 | E-GEOD-44663 | biostudies-arrayexpress
Project description:The Dahl salt-sensitive (S) rat model develops chronic hypertensive disease when fed a high salt diet that ultimately results in renal and heart failure, as well as prevalent cerebrovascular pathologies. Phenotypic changes in the cerebral vasculature are preceded by changes in gene expression, and evidence supports a role for extracellular signal-regulated kinase 1/2 (ERK1/2) in vascular cell proliferation, yet little is known regarding ERK1/2 âregulated gene transcription in cerebrovascular smooth muscle during hypertension. Findings presented here support the hypothesis that salt-induced hypertensive disease results in upregulation of ERK1/2 activity and ERK1/2-regulated genes that promote remodeling in cerebral resistance arteries. Dahl S rats were fed either a 0.4% NaCl (low salt, LS) or 8% NaCl (high salt, HS) diet until evidence of left ventricular dysfunction. Gene expression profiling using oligonucleotide array analysis detected a significant fold-change of 1.5 or greater in 133 out of 15,923 genes examined. Mitogen-activated protein kinase (MAPK)-regulated genes were overrepresented and provided a link to genes involved in proliferation and extracellular matrix signaling including plasminogen activator inhibitor I (PAI-1), osteopontin (OPN) and junB. These data suggests that salt induced hypertensive disease promotes hyperplasia and changes in matricellular genes that are likely important in vascular remodeling. Experiment Overall Design: Analysis was based on a comparison between the Low Salt and High Salt groups. Arteries from 3 animals were pooled for each sample, thus there were 9 animals/group. Analysis of significance amongst all genes as well as prospective hypotheses correlating to disease were performed.
2008-06-13 | E-GEOD-5488 | biostudies-arrayexpress
Project description:Vascular smooth muscle cells require beta1 integrin for survival. Following the induced deletion of smooth muscle beta1 integrin, smooth muscle cells undergo apoptosis and arteries become fibrotic. This microarray study on mesenteric arteries 2 weeks after the initiation of beta1 integrin deletion specifically in smooth muscle cells of the adult mouse aimed to examine early changes in expression following deletion.
2013-02-26 | GSE44663 | GEO
Project description:Background: The vascular wall of small arteries is heavily affected by high blood pressure. However, the underlying mechanisms causing vascular changes are not fully elucidated. Using a novel data-independent acquisition mass spectrometry (DIA-MS) approach, we aimed to determine the proteomic changes in small mesenteric arteries during early-onset high blood pressure in a rat model of hypertension. Methods: Snap frozen small mesenteric and renal arteries from the spontaneous hypertension rat (SHR) model and Wistar Kyoto (WKY) control rats were collected from two time points (6- and 12-weels of age) and analyzed by a label free quantitative DIA-MS workflow. Mesenteric arteries from Wister Hannover rats were included as an additional control to clarify genetic drift caused by selective inbreeding. Results: We identified a total of 3956 consistent proteins in the mesenteric artery wall and found that 286 proteins were significantly regulated in 12-weeks old SHRs compared to WKY controls. Comparing to an in silico matrisome database, we identified 38 extracellular matrix-associated proteins that could distinguish SHRs from WKY controls. Furthermore, when comparing the significantly regulated proteins identified in mesenteric and renal arteries, we identified 18 proteins, including Serpina3l, Igg-2a, ENSRNOG00000049829, Acyp2, Enpp3, Lss, Acaa1a, Basp1, an isoform of Basp1, Flot1, Flot2, Gstt1, Nit1, Ppid, Ikbkap, Poglut3, P4ha2 and Usp15, that were changed in both vascular beds. These proteins were associated with vital cellular processes, such as dyslipidemia, protease inhibition, remodeling and generation of reactive oxygen species. Majority of the identified proteins and pathways were associated with hypertension, and mapping the underlying changes help understanding the pathological processes occurring in the arterial wall during early-onset hypertension. Conclusions: Our data provides an in-depth analysis of the proteomic architecture of the mesenteric and renal artery wall from SHRs and WKY control rats. We identified 18 novel candidate proteins that highlights critical changes in small arteries of the SHR.
2022-01-06 | PXD026051 | Pride
Project description:This study used Deep RNA sequencing to define gene expression in the small resistance arteries and compare to a reference conduit artery, the aorta Methods: Deep RNA Sequencing (~90 million reads) was performed on 2 samples of adult SD rat mesenteric arteries and compared to that of 2 samples of aorta. Results: ~900 genes were identified that were expressed at least 2-fold difference between meseteric artery and aorta mRNA profiles of 2 samples of rat mesenteric artery and 2 samples of rat aorta were sequenced using Illumina HiSeq
2015-07-13 | E-GEOD-64450 | biostudies-arrayexpress