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Expression data from female rat kidney: pathophysiology of proteinuria

ABSTRACT: This study was designed to investigate gene expression in kidneys of adult female Sabra rats (SBH/y and SBN/y rat strains) with two indwelling kidneys or after uni-ninephrectomy, seeking those genes that are differentially expressed between the two strains, and between animals with one or two kidneys. SBH/y after uninephrectomy develop proteinuria to a much greater extent than SBN/y. The study was performed as part of an overall effort to detect the genes that are associated with the pathophysiology of proteinuria. Keywords: Analysis of genes that are differentially expressed in the kidneys, contrasting between an animal strain that tends to develop proteinuria which is amplified by uninephrectomy and another strain that is relatively resistant to the development of proteinuria

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE14666 | GEO | 2009/01/31

SECONDARY ACCESSION(S): PRJNA114421

REPOSITORIES: GEO

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Expression data from male rat kidney: pathophysiology of proteinuria

Project description:This study was designed to investigate gene expression in kidneys of adult Sabra rats (SBH/y and SBN/y rat strains) with two indwelling kidneys or after uni-ninephrectomy, seeking those genes that are differentially expressed between the two strains, and between animals with one or two kidneys. SBH/y after uninephrectomy develop proteinuria to a much greater extent than SBN/y. The study was performed as part of an overall effort to detect the genes that are associated with the pathophysiology of proteinuria. Keywords: Analysis of genes that are differentially expressed in the kidneys, contrasting between an animal strain that tends to develop proteinuria which is amplified by uninephrectomy and another strain that is relatively resistant to the development of proteinuria The experiment was performed in male animals after weaning. Four groups were studied: SBN/y with 2 kidneys (ham uni-nephrectomy), SBN/y after uni-nephrectomy, SBH/y with 2 kidneys (sham uninephrectomy) and SBH/y after uni-nephrectomy. Animals were provided rat chow ad libitum. At age 4 months, 3 months after uninephrectomy or sham operation, animals were sacrificed under ether anesthesia, killed by exsanguination and the kidneys were rapidly removed and snap frozen with liquid nitrogen. The kidneys were stored at -800C until RNA was extracted for the differentiale xpression experiment.

2009-02-03 | E-GEOD-14676 | biostudies-arrayexpress

Expression data from male rat kidney: pathophysiology of proteinuria

2009-02-03 | GSE14676 | GEO

Expression data from female rat kidney: pathophysiology of proteinuria

Project description:This study was designed to investigate gene expression in kidneys of adult female Sabra rats (SBH/y and SBN/y rat strains) with two indwelling kidneys or after uni-ninephrectomy, seeking those genes that are differentially expressed between the two strains, and between animals with one or two kidneys. SBH/y after uninephrectomy develop proteinuria to a much greater extent than SBN/y. The study was performed as part of an overall effort to detect the genes that are associated with the pathophysiology of proteinuria. Keywords: Analysis of genes that are differentially expressed in the kidneys, contrasting between an animal strain that tends to develop proteinuria which is amplified by uninephrectomy and another strain that is relatively resistant to the development of proteinuria The experiment was performed in female animals after weaning. Four groups were studied: SBN/y with 2 kidneys (sham uni-nephrectomy), SBN/y after uni-nephrectomy, SBH/y with 2 kidneys (sham uninephrectomy) and SBH/y after uni-nephrectomy. Animals were provided rat chow ad libitum. At age 5 months, 4 months after uninephrectomy or sham operation, animals were sacrificed under ether anesthesia, killed by exsanguination and the kidneys were rapidly removed and snap frozen with liquid nitrogen. The kidneys were stored at -800C until RNA was extracted for the differential expression experiment.

2009-01-31 | E-GEOD-14666 | biostudies-arrayexpress

Renal gene expression in uninephrectomized diabetic OVE26 mice

Project description:OVE26 (OVE) mice provide a useful model of advanced diabetic nephropathy (DN) with respect to albuminuria and pathologies. We showed that albuminuria, reduced GFR and interstitial fibrosis, which normally take 8-9 months to develop, are more advanced in uninephrectomized OVE mice within 10 weeks of surgery, at 4.5 months of age. The accelerated progression of renal damage, especially renal fibrosis in OVE-uni mice, was also identified at the gene expression level. The hepatic fibrosis/hepatic stellate cell activation pathway was by far the most significant Ingenuity canonical pathway identified by gene array in OVE-uni mice. Many inflammatory- and immune-related pathways were found among the top pathways up-regulated in OVE-uni kidneys, including acute-phase response signaling, leukocyte extravasation, IL6, IL10, IL12 signaling, TREM1 signaling, dendritic cell maturation and the complement system. These pathways were also dramatically up-regulated in 8-month-old OVE mice (GSE20636). Nephrectomized OVE mice are a much faster alternative model for studying advanced renal disease in diabetes. Study of renal gene expression in diabetic OVE26 mice. Uninephrectomy was used as an accelerating factor. Pooled RNA samples from 4 individual mice in each treatment group (OVE-uni, OVE-sham, FVB-uni, FVB-sham) were used for probe hybridization. Treatment groups: OVE-uni: uninephrectomy treatment in diabetic mice OVE-sham: sham surgery treatment in diabetic mice FVB-uni: uninephrectomy treatment in nondiabetic mice FVB-sham: sham surgery treatment in nondiabetic mice

2011-04-15 | E-GEOD-21448 | biostudies-arrayexpress

Expression data from rat kidney: pathophysiology of proteinuria

Project description:This SuperSeries is composed of the following subset Series: GSE14666: Expression data from female rat kidney: pathophysiology of proteinuria GSE14676: Expression data from male rat kidney: pathophysiology of proteinuria Refer to individual Series

2009-02-03 | E-GEOD-14677 | biostudies-arrayexpress

Transcriptional profiling of mouse glomerulus in lipopolysaccharide-induced proteinuria model

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

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

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

Sirt6 Deficiency Exacerbates Podocyte Injury and Proteinuria through Targeting Notch Signaling

Project description:Podocyte injury is a major determinant in proteinuric kidney disease and identification of potential therapeutic targets for preventing podocyte injury has clinical importance. Here, we show that histone deacetylase Sirt6 protects against podocyte injury through epigenetic regulation of Notch signaling. Sirt6 is downregulated in renal biopsies from patients with podocytopathies and its expression negatively correlates withglomerular filtration rate. Podocyte-specific deletion of Sirt6 exacerbates podocyte injury and proteinuria in two independent mouse models including diabetic nephropathy and adriamycin-induced nephropathy. Sirt6 has pleiotropic protective actions in podocytes including anti-inflammatory and anti-apoptotic effects, is involved in actin cytoskeleton maintenance, and promotes autophagy. Sirt6 also reduces urokinase plasminogen activator receptor expression, which is a key factor for podocyte foot process effacement and proteinuria. Mechanistically, Sirt6 inhibits Notch1 and Notch4 transcription by deacetylating the histone H3K9. We suggest Sirt6 as a potential therapeutic target in proteinuric kidney disease.

2017-06-20 | GSE100185 | GEO

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