Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Increased Susceptibility to AKI in a Mouse Model of Presymptomatic Cardiomyopathy

ABSTRACT: The early events that signal renal dysfunction in presymptomatic heart failure are unclear. To evaluate this, we performed RNA-seq on kidneys from transgenic mice with cardiac-specific overexpression of mutant alpha-B-crystallin, which develop slowly progressive cardiomyopathy. Presymptomatic transgenic mice display an increase in serum creatinine and in urinary neutrophil gelatinase-associated lipocalin (NGAL), but lack chronic interstitial fibrosis. Presymptomatic transgenic mouse kidneys exhibited a worsened response to ischemia-reperfusion injury based on serum creatinine, urine NGAL, tubule dilation and cast score, and apoptosis. Our findings demonstrate functional renal impairment, urinary biomarker elevations, and gene expression changes that occur in early presymptomatic heart failure, which dramatically increase the susceptibility to subsequent acute kidney injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE99703 | GEO | 2018/02/16

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptional profiling of kidneys from ADTKD-UMOD mouse model

Project description:To gain insight into autosomal dominant tubulointerstitial kidney disease (ADTKD)-uromodulin (UMOD) pathophysiology, we carried out transcriptional profiling of kidneys from 1- and 2-month-old TgUmodC147W mice, a transgenic model that recapitulates the main features of the disease, and TgUmodwt mice, a matched transgenic control of Umod overexpression. These time points correspond to presymptomatic stages that precede renal dysfunction in TgUmodC147W mice.

2017-08-18 | GSE97093 | GEO

Serum and urinary proteomes between healthy dogs and dogs with renal dysfunction in babesiosis using label-based high-resolution quantitative proteomics

Project description:The aim of the study was to analyse differences in serum and urinary proteomes between healthy dogs and dogs with renal dysfunction in babesiosis using label-based high-resolution quantitative proteomic approach. In the study 8 healthy control dogs (group H) and 22 dogs with naturally occurring babesiosis were enrolled. Dogs with babesiosis were divided into 3 groups: group A consisted of 6 non-azotaemic dogs (serum creatinine <140 μmol/L) with normal UPC (UPC < 0.5), group B of 10 non-azotaemic dogs with proteinuria (UPC > 0.5) and group C of 6 azotaemic dogs (serum creatinine > 140 μmol/L) and significant proteinuria (UPC > 2).

2022-10-18 | PXD017263 | Pride

Gene expression profile in sciatic nerve from presymptomatic SOD1G93A Amyotrophic Lateral Sclerosis animal model

Project description:Microarray analyses using a whole mouse genome platform were employed in the evaluation of gene expression pattern of sciatic nerves of transgenic SOD1(G93A) mice and their littermate controls at presymptomatic age of 60 days.

2015-06-04 | GSE69450 | GEO

Gene expression profiling of muscles from transgenic humanSODG93A mice at presymptomatic stage

Project description:The transgenic mice expressing the human mutated form (G93A) of the SOD1 gene represent a valuable model of Amyotrophic Lateral Sclerosis (ALS). SOD1 is one of the main causative genes of familial ALS which accounts for 10% of cases. These transgenic animals develop a motorneuronal pathology that recapitulates well the neuropathological features occuring in ALS patients, and the progression of the disease can be monitored by a series of motor tests. Gastrocnemius is the first and most affected muscle in the disease, while triceps is relatively spared. Gene expression data of degenerating motor neurons at different disease stages are already available, while gene expression data on the muscle tissue are missing. Our aim is to define the role of muscle in motor neuron degeneration in ALS. Keywords: Single stage analysis (presymptomatic stage, 7 week-old mice) We considered two sets of muscle at presymptomatic stage (7 weeks): gastrocnemius and triceps from 4 transgenic SOD1G93A and 4 non-transgenic mice (NTg).

2010-03-04 | E-GEOD-16360 | biostudies-arrayexpress

Expression data of the kidney tissues from wildtype and Tet2 KO mice

Project description:Our previous study has showed Ten-eleven translocation (Tet2) gene expression as well as the global 5-hydroxymethylcytosine (5hmC) level were reduced significantly in mouse kidney insulted by ischemia reperfusion (IR). Here, we investigate the functional role of Tet2 in renal IR injury. We constructed renal IR injury model in wild type and Tet2 knockout (KO) mice. Serum creatinine (SCr) and blood urea nitrogen (BUN) were examined to evaluate renal function. HE staining and renal injury biomarkers were tested to confirm the degree of injury. Microarray analysis of mRNA expression levels was carried out to gain mechanistic insightinto the role of Tet2. We used microarrays to profile the transcriptomes of the kidneys from wildtype and Tet2 KO mice.

2018-07-12 | GSE116911 | GEO

Expression data from injured murine kidney

Project description:Renal recovery following injury relies on cellular regeneration. In the mouse kidney following injury, injured epithelial cells undergoes de-differentiate, proliferate and re-differentiate into functional cells, following a a tightly controlled genetic programme where specific sets of genes are up-regulated. We used microarrays to detail the global programme of gene expression underlying cellular regeneration following injury with or without a HDAC inhibitor, m4PTB, treatment and identified distinct classes of up-regulated genes during this process. Male BALB/c mice underwent 26 minute unilateral ischemia-reperfusion (IR) with contralateral nephrectomy treated with vehicle or 100 mg/kg m4PTB 24 h after inducing renal injury, and kidneys harvested for RNA extraction 12 h later. We sought to obtain kidneys within a similar degree of injury in order to carefully evaluate the effect of m4PTB on expression profiles. To that end, we selected kidneys according to three different criteria of injury: (1) level of serum creatinine at Day1, (2) the level of blood urea nitrogen (BUN) (3) Kim1 expression by qPCR at Day1.5 using haevested kidneys

2013-03-01 | E-GEOD-42247 | biostudies-arrayexpress

Single-cell transcriptional profiles in glomeruli from type 2 db-/- mice

Project description:Diabetic nephropathy is a chronic complication of diabetes, presenting albuminuria at an early stage and leading to renal failure. Kidney is a complicated organ, which is responsible for body fluids control, acid-base balance, and removal of toxins. To better understand the progress of diabetic nephropathy, mice renal cortex of control mice, six-week db-/- (increased serum glucose without pathological changes in kidneys), and ten-week db-/- (with pathological changes in kidneys) were collected for single-cell sequencing analyses. A subgroup of glomerular endothelial cells with pro-angiogenetic features was identified in diabetic kidneys.

2023-10-27 | GSE206015 | GEO

Molecular Basis of Renal Adaptation in a Murine Model of Congenital Obstructive Nephropathy

Project description:Congenital obstructive nephropathy is a common cause of chronic kidney disease and a leading indication for renal transplant in children. The cellular and molecular responses of the kidney to congenital obstruction are incompletely characterized. In this study, we evaluated global transcription in kidneys with graded hydronephrosis in the megabladder (mgb-/-) mouse to better understand the pathophysiology of congenital obstructive nephropathy. Three primary pathways associated with kidney remodeling/repair were induced in mgb-/- kidneys independent of the degree of hydronephrosis. These pathways included retinoid signaling, steroid hormone metabolism, and renal response to injury. Urothelial proliferation and the expression of genes with roles in the integrity and maintenance of the renal urothelium were selectively increased in mgb-/- kidneys. Ngal/Lcn2, a marker of acute kidney injury, was elevated in 36% of kidneys with higher grades of hydronephrosis. Evaluation of Ngalhigh versus Ngallow kidneys identified the expression of several novel candidate markers of renal injury. This study indicates that the development of progressive hydronephrosis in mgb-/- mice results in renal adaptation that includes significant changes in the morphology and potential functionality of the renal urothelium. These observations will permit the development of novel biomarkers and therapeutic approaches to progressive renal injury in the context of congenital obstruction. Gene expression was measured in control, mild, moderate and severely hydronephrotic megabladder mouse kidneys. A total of 6 control kidneys were compared to 18 mutant kidneys from age-matched male animals.

2013-06-18 | E-GEOD-48041 | biostudies-arrayexpress

Molecular Basis of Renal Adaptation in a Murine Model of Congenital Obstructive Nephropathy

2013-06-18 | GSE48041 | GEO

Influence of retinol on kidney in 5/6 nephrectomy mice

Project description:The circadian clock has been found to be associated with various diseases. We showed that 5/6 nephrectomy (5/6Nx) Clk/Clk mice, which show mutation in the gene encoding circadian locomotor output cycles (Clock) do not show aggravation of renal fibrosis because transforming growth factor-1 (Tgf-1) expression is not increased. In wild-type 5/6Nx kidneys, we found that retinoid, a metabolite of retinol, led to alteration of the expresion 24-h rhythm of Clock expression. Renal Tgf- 1 expression is activated by Clock and further aggravates renal dysfunction by causing fibrosis. We also showed that, in 5/6Nx mice fed a retinol-free diet, renal fibrosis and apoptosis are reduced, leading to a marked improvement in serum creatinine levels. Moreover, our study identified hepatic Cyp3a11 and Cyp26a1 as key retinol metabolism-related genes whose expression decreased in 5/6Nx mice. Our data indicated that the negative chain reaction of metabolic clock alteration in between the kidney and liver aggravates renal dysfunction.

2014-06-06 | GSE57799 | 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