Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA93681 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Renal medullary genes in salt-sensitive hypertension
| PRJNA93713 | ENA
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
Project description:We analyzed the glomerular proteome in Dahl salt sensitive rats after 21 days of induction of hypertension, after 7 days and in control conditions.
2019-11-20 | PXD007937 | Pride
Project description:Microarray analysis of the development of proteinuria in the Dahl salt-sensitive rat
| PRJNA110581 | ENA
Project description:Mlycd (malonyl-CoA decarboxylase) is a regulator of fatty acid metabolism. Lysine supplementation depletes kidney malonyl-CoA in hypertensive Dahl SS rats. As a key regulatory mechanism, lysine malonylation influences mitochondrial enzymes and fatty acid metabolism, with implications for CKD, hypertension, and other disorders. Yet how the balance between malonylation and acetylation is altered, and how this affects salt-sensitive hypertension, remains unclear. In this study, we examined the proteomic and metabolomic alterations resulting from Mlycd deficiency in Dahl salt-sensitive rats. This dataset contains proteomic profiles of heart, kidney, liver tissues as well as plasma and urine samples obtained from both Mlycd+/+ and Mlycd+/- animals.
2025-12-14 | PXD062350 | Pride
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
Project description:We perfomred sc RNA seq of intetinal immun cell and PBMCs to figure out the roles of intestine in development of salt-sensitive hypertension. We fed a high salt diet(4% NaCl) or a normal salt diet(0.2% NaCl) to Dahl-salt senstive rats for 4 weeks. We isolated immune cells from small instesinal lamin propria and blood.
2025-07-23 | GSE293074 | GEO
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
Project description:Serum and glucocorticoid-induced kinase 1 (SGK1) activates the epithselial 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.
2007-10-11 | E-GEOD-599 | biostudies-arrayexpress