Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional profiling of mouse glomerulus in lipopolysaccharide-induced proteinuria model

ABSTRACT: The pathogenic mechanisms of common kidney glomerular diseases, including the vast majority of cases of proteinuria, remain unknown. To gain insight into the pathogenesis of proteinuria development, we characterized the glomerular gene expression changes that accompany early stages of proteinuria induced by lipopolysaccharide (LPS) in mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE12599 | GEO | 2009/08/26

SECONDARY ACCESSION(S): PRJNA112853

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 mouse glomerulus in lipopolysaccharide-induced proteinuria model

Project description:The pathogenic mechanisms of common kidney glomerular diseases, including the vast majority of cases of proteinuria, remain unknown. To gain insight into the pathogenesis of proteinuria development, we characterized the glomerular gene expression changes that accompany early stages of proteinuria induced by lipopolysaccharide (LPS) in mice. Nine-week-old female C57Bl6 mice were allocated to LPS-treated group (n=6) or PBS control group (n=4), and subsequently treated either by a single intraperitoneal injection LPS or control buffer.

2009-08-25 | E-GEOD-12599 | biostudies-arrayexpress

Glucocorticoid- and Pioglitazone-Induced Proteinuria Reduction in Experimental Nephrotic Syndrome Both Correlate with Glomerular ECM Modulation

Project description:Idiopathic nephrotic Syndrome (NS) is a common glomerular disease. While glucocorticoids (GC) are the primary treatment, the PPARγ agonist pioglitazone (Pio) also reduces proteinuria in patients with NS and directly protects podocytes from injury. Since both drugs reduce proteinuria, we hypothesized these effects result from overlapping transcriptional patterns. Systems biology approaches compared glomerular transcriptomes from rats with PAN-induced NS treated with GC vs. Pio and identified 29 commonly regulated genes-of-interest, primarily involved in extracellular matrix (ECM) remodeling. Correlation with clinical idiopathic NS patient datasets confirmed glomerular ECM dysregulation as a potential mechanism of injury. Cellular deconvolution in silico revealed GC- and Pio-induced amelioration of altered genes primarily within podocytes and mesangial cells. While validation studies are indicated, these analyses identified molecular pathways involved in the early stages of NS (prior to scarring) suggesting that targeting glomerular ECM dysregulation may enable a future non-immunosuppressive approach for proteinuria reduction in idiopathic NS.

2024-12-01 | GSE248053 | GEO

Spatiotemporal landscape of kidney tubular responses to glomerular proteinuria

Project description:Spatiotemporal landscape of kidney tubular responses to glomerular proteinuria

| PRJNA903394 | ENA

SMPDL3b in Podocytes: Decoupling Proteinuria from CKD Progression in Experimental Alport Syndrome

Project description:Alport Syndrome (AS) is a rare genetic disease with impaired production of collagen type IV alpha 3, 4 and 5 chains in the glomerular basement membranes (GBM), which results amongst others in progressive loss of kidney function. In AS, abnormalities in the GBM and associated podocyte detachment may potentially result from the dysregulation of sphingolipid metabolism. Here we investigated whether renal sphingomyelin phosphodiesterase acid-like 3b (SMPDL3b) overexpression modulates the generation of sphingosine-1-phosphate (S1P) and contributes to renal failure in Col4a3 knockout mice, a mouse model of AS. We found a 3-fold increase in SMPDL3b expression in glomeruli and murine podocytes isolated from Col4a3 knockout mice. Increased SMPDL3b expression occurred in association with increased glomerular S1P levels, while podocyte specific Smpdl3b deletion in Col4a3 knockout mice was sufficient to restore S1P levels and to reduce proteinuria and podocyte foot process but not sufficient to protect from renal failure. Thus, podocyte S1P may be a key modulator of proteinuria and podocyte integrity in AS. Our study in experimental AS suggests that SMPDL3b-derived S1P may dissociate proteinuria from renal failure, and suggests that improvement of glomerular structure and function may not always translate in protection from CKD progression in AS.

2024-12-19 | GSE274298 | GEO

Microarray analysis of the development of proteinuria in the Dahl salt-sensitive rat

Project description:To get more insight in cause and consequences of proteinuria, we studied glomerular gene expression patterns before and after the onset of increased urinary albumin excretion in a proteinuric rat strain. Spontaneously proteinuric Dahl salt-sensitive rats (Dahl SS) were compared to non-proteinuric, spontaneously hypertensive rats (SHR). In Dahl SS, UAE significantly increased starting from week 5 of age. Glomerular RNA profiles of 4- and 6 week-old rats were studied by Affymetrix microarrays. Keywords: Time course analysis

2009-01-01 | GSE13810 | GEO

Transcription profiling of rat Dahl salt-sensitive strain development of proteinuria

2009-01-14 | E-GEOD-13810 | biostudies-arrayexpress

Spatiotemporal landscape of kidney tubular responses to glomerular proteinuria

Project description:Proteinuria is a cardinal feature of glomerular diseases and an important risk factor for tubulo-interstitial damage, progressive decline in kidney function, and cardiovascular complications, but the precise effects of proteinuria on tubules were previously unclear. Here, using an established mouse model of glomerulopathy, single cell sequencing, in vivo imaging and other complementary methods, we investigate in detail the spatiotemporal landscape of genetic responses to increased protein filtration along the nephron. We show that proteinuria is a potent modulator of cell signaling in tubules, and triggers extensive genetic reprogramming in distal segments, with activation of numerous developmental pathways, and a generalized convergence and loss of differentiation markers. Meanwhile, in the proximal tubule - where filtered proteins are normally endocytosed and degraded - we find that encroachment of protein uptake from early (S1) into later (S2) segments causes substantial remodeling of the latter, with dramatic downregulation of canonical processes such as organic anion/uremic toxin secretion and lipid metabolism, and a concomitant increase in reabsorptive markers. Thus, we demonstrate that the tubular effects of proteinuria are extensive, pleotropic and segment specific. Moreover, we identify protein exposure as an important environmental cue that shapes the axial topography of the nephron. Taken together, these findings could explain some well recognized phenomena in humans with chronic kidney disease (CKD).

2024-05-06 | GSE218376 | GEO

Lipopolysaccharide-stimulated neutrophils

Project description:Neutrophil gene transcription following lipopolysaccharide exposure. Microarray analysis of lipopolysaccharide-treated human neutrophils. Neutrophils respond to infection by degranulation, release of reactive oxygen intermediates, and secretion of chemokines and cytokines; however, activation of neutrophil transcriptional machinery has been little appreciated. Recent findings suggest that gene expression may represent an additional neutrophil function after exposure to lipopolysaccharide (LPS). We performed microarray gene expression analysis of 4,608 mostly nonredundant genes on LPS-stimulated human neutrophils. Analysis of three donors indicated some variability but also a high degree of reproducibility in gene expression. Twenty-eight verifiable, distinct genes were induced by 4 h of LPS treatment, and 13 genes were repressed. Genes other than cytokines and chemokines are regulated; interestingly, genes involved in cell growth regulation and survival, transcriptional regulation, and interferon response are among those induced, whereas genes involved in cytoskeletal regulation are predominantly repressed. In addition, we identified monocyte chemoattractant protein-1 as a novel LPS-regulated chemokine in neutrophils. Included in these lists are five clones with no defined function. These data suggest molecular mechanisms by which neutrophils respond to infection and indicate that the transcriptional potential of neutrophils is greater than previously thought. Keywords: repeat sample

2003-03-10 | GSE105 | GEO

Lipopolysaccharide-stimulated neutrophils

2010-06-05 | E-GEOD-105 | biostudies-arrayexpress

Anti-lipopolysaccharide antibody ruminal administration mitigates the ruminal lipopolysaccharide release without acute phase inflammatory and hepatic transcriptomic responses during the subacute ruminal acidosis challenge in Holstein bull cattle

Project description:The effects of anti-lipopolysaccharide (LPS) antibody on ruminal fermentation, LPS activity, and liver transcriptomes were investigated during the subacute ruminal acidosis (SARA) challenge.

2020-05-15 | GSE150553 | 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