Ontology highlight
ABSTRACT:
PROVIDER: PRJNA766530 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16080331_1.fastq.gz | Fastqsanger.gz | |||
| SRR16080331_2.fastq.gz | Fastqsanger.gz | |||
| SRR16080332_1.fastq.gz | Fastqsanger.gz | |||
| SRR16080332_2.fastq.gz | Fastqsanger.gz | |||
| SRR16080333_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Calcitriol ameliorates damage in high-salt diet-induced hypertension: evidence of communication with the gut–kidney axis
| PRJNA766639 | ENA
Project description:Several studies have established a link between high-salt diet, inflammation, and hypertension. Vitamin D supplementation has shown anti-inflammatory effects in many diseases; gut microbiota is also associated with a wide variety of cardiovascular diseases, but potential role of vitamin D and gut microbiota in high-salt diet-induced hypertension remains unclear. Therefore, we used rats with hypertension induced by a high-salt diet as the research object and analyzed the transcriptome of their tissues (kidney and colon) and gut microbiome to conduct an overall analysis of the gut–kidney axis. We aimed to confirm the effects of high salt and calcitriol on the gut–kidney immune system and the composition of the intestinal flora. We demonstrate that consumption of a high-salt diet results in hypertension and inflammation in the colon and kidney and alteration of gut microbiota composition and function. High-salt diet-induced hypertension was found to be associated with seven microbial taxa and mainly associated with reduced production of the protective short-chain fatty acid butyrate. Calcitriol can reduce colon and kidney inflammation, and there are gene expression changes consistent with restored intestinal barrier function. The protective effect of calcitriol may be mediated indirectly by immunological properties. Additionally, the molecular pathways of the gut microbiota-mediated BP regulation may be related to circadian rhythm signals, which needs to be further investigated. An innovative association analysis of the microbiota may be a key strategy to understanding the association between gene patterns and host.
2021-10-12 | GSE184844 | GEO
Project description:The Dahl salt-sensitive (SS) rat is an established model of hypertension and renal damage that is accompanied with an activation of the immune system in the response to a high salt diet. Investigations into the effects of sodium-independent and –dependent components of the diet were shown to affect the disease phenotype with Dahl SS/JrHsdMcwi (SS/MCW) rats maintained on a purified diet (AIN-76A) presenting with a more severe phenotype relative to the grain-fed Dahl SS/JrHsdMcwiCrl rat (SS/CRL). Recently, T cells isolated from the kidneys of the two strains unveiled that transcriptomic and functional differences may contribute to the susceptibility of hypertension and renal damage. Since contributions of the immune system, environment and diet are documented to alter this phenotype, this present study examined the epigenetic profile of T cells isolated from the periphery and the kidney from these strains. In response to high salt challenge, the methylome of T cells isolated from the kidney of SS/MCW exhibit significantly more differentially methylated regions with a preference for hypermethylation compared to the SS/CRL kidney T cells. Circulating T cells exhibited similar methylation profiles between the strains. Utilizing transcriptomic data from T cells isolated from the same animals upon which the DNA methylation analysis was performed, a predominant negative correlation was observed between gene expression and DNA methylation in all groups. Lastly, inhibition of DNA methyltransferases blunted salt-induced hypertension and renal damage in the SS/MCW rats providing a functional role for methylation. The study demonstrated the influence of epigenetic modifications to immune cell function, highlighting the need for further investigations.
2019-06-10 | GSE132417 | GEO
Project description:Hypertension and kidney disease, two related, common, and severe disease entities have been repeatedly associated with genomic variants and metabolic alterations of lysine metabolism. Here, we developed a stable isotope labeling strategy compatible with untargeted metabolomics acquisition to investigate the physiology and molecular spectrum of lysine’s metabolic fate in vivo. Mice received 13C6 labeled lysine through the diet over two months to track more than 100 lysine metabolites across various organs and body fluids. Globally, lysine reacts rapidly with molecules of the central carbon metabolism, as opposed to slow or incorporation into proteins and metabolization into acylcarnitines. Lysine metabolism is accelerated in the rat model of the Dahl salt-sensitive hypertension and kidney damage, chiefly through N-alpha-mediated degradation. Here, lysine administration completely diminished the development of salt-sensitive hypertension and kidney injury. Administration of lysine leads to diuresis, even further acceleration of 13C6 lysine conjugate formation, and inhibition of albumin uptake, thereby protecting from nephron injury and metabolic stress. Lysine conjugates with malonyl-CoA to form a novel metabolite N-malonyl-lysine, to deplete malonyl-CoA from fatty acid synthesis. This process occurs at the expense of protein malonylation. In hypertensive rats with kidney damage, lysine molecules were excreted as fructoselysine, saccharopine and Nε-acetyllysine, via the urine, leading to an overall depletion of central carbon metabolites from the organism and kidney. Consistent with findings in the salt-sensitive rat, lysine challenge of patients with mild kidney damage inhibited tubular albumin uptake, increased lysine conjugate formation in the urine, and reduced TCA cycle metabolites, in contrast to kidney-healthy volunteers. In conclusion, comprehensive lysine isotope tracing mapped an accelerated lysine metabolism in hypertension, and further, lysine administration induced kidney protection in kidney disease.
2022-06-01 | PXD029232 | Pride
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 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 wanted to understand how a salt restriction diet could improve cardiac damage (ie cardiac hypertrophy, fibrosis, hypertension) in a rat model of metabolic syndrome. We thus performed an Agilent microarray experiment in order to identify expression variations in left ventricles of rats having a normal sodium diet (0,64%) or a low sodium diet (less than 0,01%)
2017-04-20 | GSE84524 | GEO
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
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
Project description:Dahl-Iwai (DI) salt-sensitive rats were studied using microarrays to identify gender-specific differences in the kidney, both basal differences and responses to a high salt diet. In DI rat kidneys, gene expression profiles demonstrated inflammatory and fibrotic responses selectively in females. Gonadectomy of DI rats abrogated gender differences in gene expression. Gonadectomized female and gonadectomized male DI rats both responded to high salt with the same spectrum of gene expression changes as intact female DI rats. Androgens dominated the gender selective responses to salt. Several androgen-responsive genes were identified with roles potentiating the differential responses to salt including increased male expression of Angiotensin-Vasopressin Receptor and Prolactin Receptor, decreased 5-alpha reductase, and mixed increases and decreases in expression of Cyp4a- genes that can produce eicosanoid hormones. These gender differences potentiate sodium retention by males, and increase kidney function during gestation by females. Keywords: Disease-State Analysis (Salt-Sensitive Hypertension)
2007-07-01 | GSE5285 | GEO