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E-MTAB-11355

ABSTRACT: Sodium accumulation and blood capillary rarefaction in the skin predispose spontaneously hypertensive rats to salt sensitive hypertension.

PROVIDER: E-MTAB-11355 | ExpressionAtlas | 2025-05-30

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-11355-analysis-methods.tsv	Tabular
	E-MTAB-11355-analytics.tsv	Tabular
	E-MTAB-11355-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-11355-configuration.xml	Xml
	E-MTAB-11355-g1_g3-mvaPlot.png	Other

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Sodium accumulation and blood capillary rarefaction in the skin predispose spontaneously hypertensive rats to salt sensitive hypertension.

Project description:Sodium accumulation and blood capillary rarefaction in the skin predispose spontaneously hypertensive rats to salt sensitive hypertension.

| PRJEB50395 | ENA

Sodium accumulation and blood capillary rarefaction in the skin predispose spontaneously hypertensive rats to salt sensitive hypertension.

Project description:We compared tissue Na+ storage in salt sensitive spontaneously hypertensive rats (SHR) versus salt resistant normotensive Brown Norway (BN) rats after salt loading (10 days drinking 1% NaCl solution), the SHR showed significant parallel increase in osmotically inactive Na+ storage in the skin while no significant changes in skin electrolyte concentrations were observed in BN rats. SHR rats after salt treatment exhibited a nonsignificant decrease in skin blood capillary number (rarefaction) while BN rats showed significantly increased skin blood capillary density. Analysis of dermal gene expression profiles in BN rats after salt treatment showed significant up-regulation of genes involved in angiogenesis and proliferation of endothelial cells contrary to the SHR.

2023-01-01 | E-MTAB-11355 | biostudies-arrayexpress

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

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

Bulk RNAseq of ex vivo salt treated isolated human monocytes

Project description:Salt sensitivity of blood pressure (SSBP) is associated with persistent immune activation after sodium normalization, suggesting immune “salt memory.” Prior work identified that sodium entry into antigen-presenting cells (APCs) via epithelial sodium channels triggers NLRP3 inflammasome activation through the formation of isolevuglandins (IsoLGs), highly reactive lipid aldehydes. IsoLG scavenging with 2-hydroxybenzylamine (2-HOBA) reduces NLRP3 expression and attenuates salt-induced hypertension, implicating IsoLGs as upstream immune regulators. This study tested whether IsoLGs also act as epigenetic modifiers by covalently modifying histone H1, thereby altering chromatin accessibility at inflammatory loci such as NLRP3. PBMCs from 10 hypertensive adults classified as salt-sensitive (SS) or salt-resistant (SR) were collected at baseline, after salt loading, and after depletion. Integrated single-cell RNA-seq and ATAC-seq revealed that SS monocytes exhibited salt-induced enhancer activation and increased chromatin accessibility at the NLRP3 locus. IsoLG–protein adducts correlated with blood pressure changes and were most prominent in CD14⁺ monocytes. In murine APCs, high salt induced IsoLG adduction of histone H1, attenuated by 2-HOBA. Knockdown of H1F0 reduced high salt–induced NLRP3 expression, supporting a role for H1.0 in transcriptional regulation. These findings identify IsoLG modification of histone H1 as a potential mechanism linking extracellular sodium exposure to persistent chromatin remodeling and sustained inflammatory gene expression in SS individuals. IsoLG–histone adducts may represent novel therapeutic targets for immune-driven hypertension.

2025-09-26 | GSE308365 | GEO

Urinary phosphate-containing nanoparticle contributes to inflammation and kidney injury in salt-sensitive hypertension

Project description:Although disturbed phosphate metabolism frequently accompanies chronic kidney disease, it is unclear whether it contributes to the progression of renal dysfunction. Here, we show that urinary phosphate-containing nanoparticles promote kidney injury in salt-sensitive hypertension. Remarkably, four weeks of high salt loading resulted in a 2.5-fold increase in urinary phosphate excretion in Dahl salt-sensitive rats on a normal phosphorus diet. Inhibition of intestinal phosphate absorption using sucroferric oxyhydroxide (SF) in this model suppressed phosphaturia, attenuating glomerulosclerosis and tubulointerstitial injury without significantly affecting serum phosphate, blood pressure, or urinary sodium levels. In the kidney, macrophage infiltration and inflammatory cytokine induction were ameliorated by SF. Additionally, macrophage infiltration but not myofibril hypertrophy was alleviated in the heart. In vitro, phosphate loading to proximal tubule cells significantly increased inflammatory cytokine Ccl2, which was abolished by the removal of phosphate-containing nanoparticles but not by the knockdown of phosphate transporter Slc34a1. Finally, transcriptome analysis revealed a potential role of complement C1q in renal inflammation associated with disturbed phosphate metabolism. These data demonstrate that increased phosphaturia promotes inflammation and renal injury from an early stage of salt-sensitive hypertension, and suggest the need for interventions against subclinical phosphate accumulation to improve the prognosis of hypertensive kidney disease.

2020-08-22 | GSE143440 | GEO

Microarray analysis of the development of proteinuria in the Dahl salt-sensitive rat

Project description:To get more insight in cause and consequences of proteinuria, we studied glomerular gene expression patterns before and after the onset of increased urinary albumin excretion in a proteinuric rat strain. Spontaneously proteinuric Dahl salt-sensitive rats (Dahl SS) were compared to non-proteinuric, spontaneously hypertensive rats (SHR). In Dahl SS, UAE significantly increased starting from week 5 of age. Glomerular RNA profiles of 4- and 6 week-old rats were studied by Affymetrix microarrays. Keywords: Time course analysis

2009-01-01 | GSE13810 | GEO

Quantitative TMT proteomics of brainstem in spontaneously hypertensive rats

Project description:The brainstem, the core of the central nervous system, plays a vital role in controlling arterial blood pressure and its elevation of hypertension subtypes, especially essential hypertension. Integrative metabolic and proteomic profiling was performed on the brainstem samples of 11-week-old spontaneously hypertensive rats (SHRs) and age-matched normotensive Wistar rats, using hydrophilic interaction liquid chromatography-quadrupole/time-of-flight mass spectrometry (HILIC-Q/TOFMS) and nano-liquid chromatography-high-resolution-mass spectrometry (nano-LC-high-resolution-MS) combined with quantitative tandem mass tags (TMT).

2020-09-24 | PXD021210 | Pride

Gene expression in a resistance artery in 2 models of hypertension in the rat

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

Integrated analysis of miRNA-mRNA interactions reveals novel target pathways in hypertension-induced cardiac remodeling (mRNA-seq dataset)

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

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