Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of Chromogranin A on renal function in a mouse model of failing kidney

ABSTRACT: Chromogranin A (CHGA) is elevated in plasma of patients with renal failure and several CHGA polymorphisms are associated with hypertensive renal disease. Therefore, we investigated the role of CHGA in kidney disease using the partial nephrectomy model of kidney failure. Mice under surgery to remove 2/3rds of the left kidney and the entire right kidney. Control mice received the sham surgery. Wild-type and CHGA-/- mice used. To model the changes in vitro, CRL-1927 kidney cells were treated with or without CHGA in vitro.

ORGANISM(S): Mus musculus

PROVIDER: GSE106300 | GEO | 2018/10/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptomic changes in response to 5/6 or 1/3 nephrectomy

Project description:We report the changes in kidney mRNA abundance in response to 5/6 nephrectomy or 1/3 nephrectomy surgery when compared to sham operated controls.

2022-03-01 | GSE194367 | GEO

Role of Chromogranin A on renal function in a mouse model of failing kidney

Project description:Role of Chromogranin A on renal function in a mouse model of failing kidney

| PRJNA416147 | ENA

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

5/6 nephrectomy (5/6Nx) effect on the brain

Project description:Chronic kidney disease (CKD) is a very important problem in global health treatment. CKD increases the disease risk of apoplexy, cardiac failure and cardiac infarction. In addition, neurological complications, including depression and restless legs syndrome, occur in almost all CKD patients; however, the mechanisms of these neurological complications remain unclear. Here, we showed the disruptive effect of chronic renal failure in 5/6 nephrectomy mice on an immobility time of forced swim and tail suspension test and the 24-hr rhythm of Drd2 and clock gene expressions in the striatum. These disruptive effects were induced by abnormal signal transduction in high TGF-M-NM-21 expression from the kidney. Abnormal TGF-M-NM-2 signal in the striatum led to TCF7L2 expression and ID2 induced by TCF7L2 led to disruption of the 24-hr rhythm of clock gene expression. These findings suggest that neurological complications in CKD might be overcome by amelioration of the TGF-M-NM-2 signal. Differential gene expression between 5/6 nephrectomized and sham-operated mouse was measured on the brain.

2013-08-01 | E-GEOD-35134 | biostudies-arrayexpress

Signaling in Renal Compensatory Hypertrophy Revealed by Multi-Omics_Outer Cortex

Project description:This mouse kidney outer cortex proteomics data set is part of multi-omic approach in a mouse unilateral nephrectomy model to identify signaling processes associated with compensatory hypertrophy of the renal proximal tubule.

2023-06-05 | PXD039697 | Pride

The changes of Chromatin Accessibiliy Triggered by Unilateral Nephrectomy [ATAC-seq]

Project description:Purpose: Experiments were done in mice undergoing unilateral nephrectomy (UNx) and sham nephrectomy. At specific time points (24 hours and 72 hours) after surgery, the earliest first portion of the kidney proximal tubule (PT-S1) and the cortical collecting duct (CCD) were manually micro-dissected and utilized for transcriptomic analysis by single-tubule small sample RNA-Seq and single-tubule ATAC seq. Methods: We carried out ATAC-sequencing in microdissected ealiest portion of proximal tubules (PT-S1) from mice with or without (sham) unilateral nephrectomy (UNx). Each group (Sham or UNx) has 3 biological replicates. Results and conclusion: ATAC-seq peaks in microdissected PT-S1 revealed a predominance of binding site motifs corresponding to PPARα.

2022-08-14 | GSE211022 | GEO

Gene expression in rat kidney following recovery from acute renal failure (ARF)

Project description:This experiment was designed to study the alteration in expression of mRNA is kidney following recovery from transient acute renal failure. The model used was a 52 min. bilateral renal artery clamping, followed by reperfusion, which resulted in a transient loss of renal function, followed by a functional recovery. All tissue in this study was harvested 35 days post-surgery, when renal function was restored, and renal structure largelyy normal. For controls, sham-operated animals were used. An N of 6 post-ischemia reperfusion animals were used with 6 sham-operated controls. For hybridization studies, RNA from one of six post-ischemic acute renal failure animals were compared with with RNA from kidney of six sham-operated control animals. Each ARF vs. sham-operated comparison was performed twice, alternating the cy3 and cy5 label between the two hybridizations for each pair. A second set of hybridizations was carried out using sham vs. sham hybridizations. This was done to get a quantitative analysis of the variation of the biological and microarry platform.

2010-06-10 | E-GEOD-1714 | biostudies-arrayexpress

Gene expression profile on ischemic kidneys from wildtype C57BL/10 and TLR4 null C57BL/10ScNJ mice

Project description:TLR4 deficiency attenuates kidney injury after ischemic reperfusion as measured by both renal function and morphology. To better understand the role of TLR4 during the acute kidney injury, we used DNA microarray to identify genes that were differentially expressed on kidneys in wildtype B10 mice and TLR4 null mice during the early stage of injury. A murine ischemic reperfusion injury model was established. After right nephrectomy, the left pedicle was clamped for 23min followed by 4hr reperfusion. Sham mice were used as controls. 6 WT males and 6 TLR4 null males were included with 3 ischemic and 3 shams in each group.

2012-08-15 | E-GEOD-34351 | biostudies-arrayexpress

Gene expression profile at bulk (24h, 48h & 72h) and single nucleus (24h) level of mouse right kidney post sham operation and unilateral nephrectomy.

Project description:The mechanism driving the remarkable ability of the remaining kidney to enlarge and increase its function following removal of its contralateral pair remains elusive. To explore the pathways driving compensatory renal hypertrophy, comprehensive RNA-seq transcriptional studies in the kidneys of mice undergoing hypertrophy 24, 48 and 72 hours following nephrectomy have been undertaken and compared with mice undergoing sham operations. The results reveal substantial time dependent enhancement of cholesterol biosynthesis pathways, increases in mitochondrial gene expression and cell cycle perturbations. Single nuclei RNA-Seq 24 hours post nephrectomy was used to further explore cholesterol biosynthesis signature and its driver SREBP2. In a cell specific manner, snRNA-seq demonstrated that SREBP2 activity increases in proximal tubules and medullary thick ascending limb and is responsible for cell size regulation following IGF-1 stimulation. These results suggest a previously undescribed role for SREBP2 in the mechanism underlying compensatory renal hypertrophy. This mechanism might be amenable to therapeutic manipulation to enhance kidney size and function.

2024-07-18 | GSE241213 | GEO

5/6 nephrectomy (5/6Nx) effect on the brain

Project description:Chronic kidney disease (CKD) is a very important problem in global health treatment. CKD increases the disease risk of apoplexy, cardiac failure and cardiac infarction. In addition, neurological complications, including depression and restless legs syndrome, occur in almost all CKD patients; however, the mechanisms of these neurological complications remain unclear. Here, we showed the disruptive effect of chronic renal failure in 5/6 nephrectomy mice on an immobility time of forced swim and tail suspension test and the 24-hr rhythm of Drd2 and clock gene expressions in the striatum. These disruptive effects were induced by abnormal signal transduction in high TGF-β1 expression from the kidney. Abnormal TGF-β signal in the striatum led to TCF7L2 expression and ID2 induced by TCF7L2 led to disruption of the 24-hr rhythm of clock gene expression. These findings suggest that neurological complications in CKD might be overcome by amelioration of the TGF-β signal.

2013-08-01 | GSE35134 | 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