Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

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. 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.

ORGANISM(S): Mus musculus

SUBMITTER: ying sun

PROVIDER: E-GEOD-12599 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Glomerular transcriptome changes associated with lipopolysaccharide-induced proteinuria.

Sun Ying Y He Liqun L Takemoto Minoru M Patrakka Jaakko J Pikkarainen Timo T Genové Guillem G Norlin Jenny J Truvé Katarina K Tryggvason Karl K Betsholtz Christer C

American journal of nephrology 20090109 6

<h4>Background</h4>Global gene expression patterns have recently been characterized in normal glomeruli, but gene expression changes that accompany glomerular disease remain poorly characterized.<h4>Method</h4>Here, we mapped global glomerular gene expression profile changes occurring in conjunction with lipopolysaccharide (LPS)-induced proteinuria in mice.<h4>Results</h4>We observed dramatic transcriptional reprogramming in glomeruli in response to LPS, representing some 20% of all genes and ab ...[more]

PMID: 19136817

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Project description:The blood-brain barrier (BBB) consists of specific physical barriers, enzymes and transporters, which together maintain the necessary extracellular environment of the central nervous system (CNS). The main physical barrier is found in the CNS endothelial cell, and depends on continuous complexes of tight junctions combined with reduced vesicular transport. Other possible constituents of the BBB include extracellular matrix, astrocytes and pericytes, but the relative contribution of these different components to the BBB remains largely unknown. Here we demonstrate a direct role of pericytes at the BBB in vivo. Using a set of adult viable pericyte-deficient mouse mutants we show that pericyte deficiency increases the permeability of the BBB to water and a range of low-molecular-mass and high-molecular-mass tracers. The increased permeability occurs by endothelial transcytosis, a process that is rapidly arrested by the drug imatinib. Furthermore, we show that pericytes function at the BBB in at least two ways: by regulating BBB-specific gene expression patterns in endothelial cells, and by inducing polarization of astrocyte end-feet surrounding CNS blood vessels. Our results indicate a novel and critical role for pericytes in the integration of endothelial and astrocyte functions at the neurovascular unit, and in the regulation of the BBB. The brain microvascular fragments were isolated from mice with different genotypes, each represented by 3-4 biological replicates. Genotypes 1-2: Platelet derived growth factor-B (PDGF-B) retention-motif knockout (pdgfbret/ret) represent the pericyte-deficient situation, and the heterozygous mice (pdgfbret/+) are used as controls. Genotypes 3-4: Hypomorphic PDGF-B mutants that rescue pdgfb-/- null mice, in which a one copy of a conditionally silent human PDGF-B transgene targeted to the Rosa 26 locus (R26P) is turned on by endothelial-specific expression of Cre recombinase. In this data set these mice are named as Tie2Cre, R26P+/0, pdgfb-/- (representing the pericyte-deficient situation). Mice wt for pdgfb (pdgfb+/+) and carrying one silent copy of R26P (R26P+/0), are used as controls. Genotype 5: Adult Notch3+/+ wildtype (WT).

Dataset Information

Transcriptional profiling of mouse glomerulus in lipopolysaccharide-induced proteinuria model

Publications

Glomerular transcriptome changes associated with lipopolysaccharide-induced proteinuria.

Similar Datasets

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