Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Salt Induced Hypertensive Disease Results in Over Expression of Matricellular Genes in Cerebral Arteries

ABSTRACT: 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

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE5488 | GEO | 2007/08/09

SECONDARY ACCESSION(S): PRJNA96125

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of rat arteries from animals with salt induced hypertensive disease results in over expression of matricellular genes in cerebral arteries

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

Mechanisms of Sinoatrial Node Dysfunction in Heart Failure with Preserved Ejection Fraction

Project description:RNA sequencing from sinoatrial node tissue was performed to identify transcriptomic changes in Dahl salt-sensitive rats fed with normal salt diet (0.4% NaCl, control group) or high-salt diet (8% NaCl, HFpEF group) for 11 weeks. Transcriptomic profiling revealed numerous changes in multiple disease-associated genes in HFpEF, which is functionally related to the observed physiological impairments and structural remodeling.

2022-05-18 | GSE184120 | GEO

Transcription profiling of rat kidney samples from Dahl salt-sensitive and Lewis strains

Project description:Male Dahl salt sensitive and Lewis rats (n=3 each) were fed an 8% NaCl diet starting at 5 weeks of age for 8 weeks. Total RNA was isolated with TRIzol reagent from DS and LEW kidneys and was subjected to microarray analysis. Experiment Overall Design: Male Dahl salt sensitive and Lewis rats (n=3 each) were fed an 8% NaCl diet starting at 5 weeks of age for 8 weeks. Total RNA was isolated with TRIzol reagent from DS and LEW kidneys and was subjected to microarray analysis. The resulting data were analyzed with GeneChip Operating Software ver1.4. Three independent experiments comparing expressions between salt-loaded Dahl salt sensitive and salt-loaded Lewis rats were performed.

2007-11-29 | E-GEOD-4800 | biostudies-arrayexpress

Circular RNAs in Rat Models of Cardiovascular and Renal diseases

Project description:The objective of this study was to profile circular RNAs (circRNAs) in rat genetic models of cardiovascular and renal disease. Renal profiles were obtained from the Dahl Salt-Sensitive rat (S), the Dahl Salt-Resistant rat (R), the Spontaneously Hypertensive Rat (SHR) and the Wistar Kyoto rat (WKY).

2017-07-27 | GSE92669 | GEO

Transcriptomic Analysis in Renal T Lymphocytes Exposes Sodium-Independent Dietary Differences in Dahl Salt-Sensitive Rats

Project description:Background. The Dahl salt-sensitive (SS) rat is an established model of salt-sensitive hypertension and renal damage. Recently, sodium-independent dietary effects were shown to be important in the development of the SS hypertensive phenotype. Compared to Dahl SS/JrHsdMcwi (SS/MCW) rats fed a purified diet (AIN-76A), grain-fed Dahl SS/JrHsdMcwiCrl rats (SS/CRL; Teklad 5L2F) were less susceptible to salt-induced hypertension and renal damage. Methods. With the known role of the immune system in hypertension, the present study characterized the immune cells infiltrating SS/MCW and SS/CRL kidneys. To further identify distinct molecular pathways between SS/MCW and SS/CRL, transcriptomic analysis was performed via RNA sequencing in T-cells isolated from the blood and kidneys of low and high salt-fed rats. Results. Following a 3-week high salt (4.0% NaCl) challenge, SS/CRL rats were protected from salt-induced hypertension (116.5±1.2 vs 141.9±14.4 mmHg) and albuminuria (21.7±3.5 vs 162.9±22.2 mg/day) compared to SS/MCW. Additionally, the absolute number of immune cells infiltrating the kidney was significantly reduced in SS/CRL. RNA-seq revealed >50% of all annotated genes in the entire transcriptome to be significantly differentially expressed in T-cells isolated from blood versus kidney. Pathway analysis of significant differentially expressed genes between SS/MCW and SS/CRL renal and circulating T-cells demonstrated salt-induced changes in genes related to inflammation in SS/MCW compared to metabolism-related pathways in SS/CRL. Conclusions. These functional and transcriptomic T-cell differences between SS/MCW and SS/CRL show that sodium-independent dietary effects may influence the immune response and infiltration of immune cells into the kidney, ultimately impacting susceptibility to salt-induced hypertension and renal damage.

2019-08-26 | GSE127000 | GEO

Identification of gene modulating vascular inflammation using chromosome 2 fragment substitutions and RNA sequencing [miRNA-Seq]

Project description:Chromosome 2 introgression from normotensive Brown Norway (BN) rats into hypertensive Dahl salt-sensitive (SS) background (consomic S2B) reduced blood pressure (BP) and vascular inflammation under normal salt diet (NSD). We hypothesized that BN chromosome 2 contains anti-inflammatory genes that could reduce BP elevation and vascular inflammation in rats fed NSD and high salt diet (HSD). We used chromosome 2 fragment substitutions to map chromosome 2 portion associated with vascular inflammation changes and next generation sequencing (NGS) to profile microRNAs in thoracic descending aorta of SS and congenic rats fed NSD or HSD.

2021-03-22 | GSE149515 | GEO

Gene expression in kidney from Lewis and Dahl(S) rat

2007-05-09 | GSE4800 | GEO

Monoclonal Antibody to Marinobufagenin Downregulates TGFβ Profibrotic Signaling in Left Ventricle and Kidney and Reduces Tissue Remodeling in Salt‐Sensitive Hypertension [LV_Kidney]

Project description:Elevated levels of an endogenous Na/K‐ATPase inhibitor marinobufagenin accompany salt‐sensitive hypertension and are implicated in cardiac fibrosis. Immunoneutralization of marinobufagenin reduces blood pressure in Dahl salt‐sensitive (Dahl‐S) rats. The effect of the anti‐marinobufagenin monoclonal antibody on blood pressure, left ventricular (LV) and renal remodeling, and LV gene expression were investigated in hypertensive Dahl‐S rats.

2022-07-12 | GSE208009 | GEO

Identification of gene modulating vascular inflammation using chromosome 2 fragment substitutions and RNA sequencing [RNA-Seq]

Project description:Chromosome 2 introgression from normotensive Brown Norway (BN) rats into hypertensive Dahl salt-sensitive (SS) background (consomic S2B) reduced blood pressure (BP) and vascular inflammation under normal salt diet (NSD). We hypothesized that BN chromosome 2 contains anti-inflammatory genes that could reduce BP elevation and vascular inflammation in rats fed NSD and high salt diet (HSD). We used chromosome 2 fragment substitutions to map chromosome 2 portion associated with vascular inflammation changes and next generation sequencing (NGS) to profile messenger RNAs (mRNAs) and non-coding RNAs (ncRNAs) in thoracic descending aorta of SS and congenic rats fed NSD or HSD.

2021-03-22 | GSE149514 | GEO

Dietary salt and renal function

Project description:Serum and glucocorticoid-induced kinase 1 (SGK1) activates the epithelial sodium channel (eNaC) in tubules. We examined renal SGK1 abundance in salt-adaptation and in salt-sensitive hypertension. Sprague-Dawley and Dahl salt-sensitive rats were placed on either 8% or 0.3% NaCl diets for 10 days. Plasma aldosterone levels were approximately 2.5-fold greater on 0.3% versus 8% NaCl diets in both rat strains. Both serum and glucocorticoid-induced kinase 1 transcript and protein abundance were less (P<0.01) in Sprague-Dawley rats and greater (P<0.01) in Dahl salt-sensitive rats on 8% versus 0.3% NaCl diets. The cDNA sequences of serum and glucocorticoid-induced kinase 1 in both strains of rat were the same. The present results provide evidence that the abundance of serum and glucocorticoid-induced kinase 1 in rat kidney may play a role in salt adaptation and the pathogenesis of hypertension and suggests that aldosterone is not the primary inducer of SGK1 in the Sprague-Dawley rat. Keywords = Rattus norvegicus, Sprague Dawley, Dahl SS/Jr, kidney, NaCl diet Keywords: other

2004-02-14 | GSE599 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data