Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Salt suppresses IFNγ-inducible chemokines in mouse kidneys with a high-salt condition

ABSTRACT: Transcriptional profiling related cytokines and chemokines of mouse kidneys comparing the kidneys of WNK4 D561A/+ mice fed an 8% high-salt diet with those of WNK4+/+ littermates with a normal diet. Goal was to determine the effects of a high-salt condition on the immune system in kidney.

ORGANISM(S): Mus musculus

PROVIDER: GSE87600 | GEO | 2017/06/12

SECONDARY ACCESSION(S): PRJNA345354

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Salt suppresses IFNγ inducible chemokines through the IFNγ-JAK1-STAT1 signaling pathway in proximal tubular cells.

Project description: Not available

| S-EPMC5397865 | biostudies-other

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

Kidneys of Dahl salt sensitive rats

Project description:Gene expression profiling of kidney tissue from 5 week old Dahl salt sensitive rats and congenic strain of Chr.10 Dahl salt sensitive rats. Keywords: other

2003-08-20 | GSE413 | GEO

Transcriptome in rat kidneys exposed to a fetal low-protein diet on postnatal days 5, 10, and 28

Project description:Early in fetal development, maternal nutritional environments are expected to induce changes in epigenetic regulation in offspring.In the present study, we integrated methylome and transcriptome data to identify potential salt-sensitive hypertension genes using the kidneys of pups exposed to a low-protein diet throughout their fetal life. We aimed to uncover how specific candidate marker genes are modified over time and under different nutritional interventions at an early age. Using the kidneys of pups exposed to a low-protein diet (LP) compared to those exposed to a control diet (CN) during fetal life, we searched for candidate genes by integrating data from both methylome and transcriptome profiling.Transcriptome analyses were used to identify genes with differential expression.

2023-10-04 | GSE215329 | GEO

Sequencing of isolated glomeruli from low salt and high salt diet fed salt sensitve Dahl rats

Project description:We report the comparison of low salt vs high salt diet fed Dahl rat kidney glomeruli by sequencing analysis

2023-09-01 | GSE237521 | GEO

Salt induces hepatic inflammatory response through epigenetic modulation of SIRT3 [ChIP-seq]

Project description:Purpose: Our previous study has confirmed that reduction of SIRT3 expression is a main factor contributing to salt-induced hepatic inflammtion. Here we sought to investigate whether salt-induced SIRT3 reduction was related to epigenetic modification. Methods: 6-week-old male SIRT3 knockout or their wild-type littermates were fed with high salt diet (HSD, containing 8% NaCl) or normal salt diet (NSD, containing 0.4% NaCl) for 4 months. And then their liver tissues were removed and subjected to ChIP-seq using antibodies against H3K27ac (ab4729), H3K4me1 (ab8895), H3K9ac (39917) and H3 (ab1791). Results: Through ChIP-seq, we observed the enrichment of H3K27ac was increased on the promoters of Sirt3 and some pro-inflammatory genes, including Ccl2, Tnf and Il6, after high salt loading. However, neither H3K4me1 nor H3K9ac displayed such phenomunum. In addition, those genes containing increased H3K27ac level in response to high salt were mainly enriched in metabolism and inflammatory pathways. And knockout of SIRT3 mainly affected genes related to AMP-activated protein kinase (AMPK) and insulin signaling pathways. Conclusions: Salt-induced SIRT3 reduction is related to the epigenetic regulation, especially H3K27ac.

2023-09-01 | GSE183582 | GEO

Salt induces hepatic inflammatory response through epigenetic modulation of SIRT3 [RNA-seq]

Project description:Purpose: Although clinical evidence suggests that high salt intake is associated with NAFLD, the underlying mechanism remains elusive. We sought to investigate whether salt-induced inflammation in liver is dependent on SIRT3 reduction. Methods: 6-week-old male SIRT3 knockout or their wild-type littermates were fed with high salt diet (HSD, containing 8% NaCl) or normal salt diet (NSD, containing 0.4% NaCl) for 4 months. And then their liver tissues were removed and total RNA was extracted to perform RNA sequencing. Results: 1850 differentially upregulated expressed genes were identified when comparing HSD group (HSD1, HSD2) to NSD group (NSD WT1, NSD2). Meanwhile, 1246 differentially upregulated expressed genes in response to SIRT3 knockout were determined (each group containing 3 samples). we observed that the common genes upregulated by both HSD and knockout of SIRT3 were enriched in immune system, including Tnf, Ccl2, etc. In addition, the common genes upregulated by knockout of SIRT3 in both NSD and HSD group were still enriched in the immune system. Conclusions: Through RNA-seq, we determined that HSD-induced hepatic inflammtion was highly similar to the effect of SIRT3 knockout, suggesting that reduction of SIRT3 expression is the main reason leading to salt-induced hepatic inflammation.

2023-09-01 | GSE183584 | GEO

Hypertensive Rat Kidney Study: Gender-Selective Responses to Salt in Dahl-Iwai & Sprague-Dawley Rats

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

Gene expression data from HeLa cells under high salt condition

Project description:We examined the role of HES1 in high salt response as a novel regulator of NFAT5. We analyzed gene expression of HeLa cells under isoosmotic and high salt condition.

2024-05-22 | GSE267676 | GEO

Gene Expression Profile in kidneys from Cldn16 +/+, +/-, -/- female mice

Project description:Claudin-16 deficiency leads to renal salt wasting in humans and mice. Analysis of renal gene expression in Claudin-16 deficient mice, compared to heterozygous and wild type littermates, was performed to gain insights into molecular mechanisms compensating salt loss. Our results indicate the upregulation of known and putative genes for renal transcellular transporters. Furthermore, we could identify a transcript so far not associated with renal salt metabolism, which will provide a first link to a human electrolyte disorder disease.

2010-02-15 | GSE19961 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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