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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from renal cortex of ICR-derived Glomerulonephritis (ICGN) mice and ICR mice

ABSTRACT: ICR-derived glomerulonephritis (ICGN) mice is a novel inbred strain of mice with a hereditary nephrotic syndrome. Deletion mutation of tensin 2 (Tns2), a focal adhesion molecule, has been suggested to be responsible for nephrotic syndrome in ICGN mice, however, existence of other associative factors has been suggested. To identify additional associative factors and to better understand onset mechanism of nephrotic syndrome in ICGN mice, comprehensive gene expression analysis using DNA microarray was conducted. Immune-related pathways were markedly altered in ICGN mice kidney as compared with ICR mice. Furthermore, gene expression level of complement component 1, s subcomponent (C1s), whose human homologue has been reported to associate with lupus nephritis, was markedly low in ICGN mice kidney. RNA from renal cortex of 4- and 8-week-old ICGN and ICR mice was extracted and processed for hybridization on Affymetrix microarrays (N=3).

ORGANISM(S): Mus musculus

SUBMITTER: Kotaro Tamura

PROVIDER: E-GEOD-45005 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from renal cortex of ICR-derived Glomerulonephritis (ICGN) mice and ICR mice

Project description:ICR-derived glomerulonephritis (ICGN) mice is a novel inbred strain of mice with a hereditary nephrotic syndrome. Deletion mutation of tensin 2 (Tns2), a focal adhesion molecule, has been suggested to be responsible for nephrotic syndrome in ICGN mice, however, existence of other associative factors has been suggested. To identify additional associative factors and to better understand onset mechanism of nephrotic syndrome in ICGN mice, comprehensive gene expression analysis using DNA microarray was conducted. Immune-related pathways were markedly altered in ICGN mice kidney as compared with ICR mice. Furthermore, gene expression level of complement component 1, s subcomponent (C1s), whose human homologue has been reported to associate with lupus nephritis, was markedly low in ICGN mice kidney.

2013-07-31 | GSE45005 | GEO

Up-regulation of prolactin receptor in the proximal tubular cells in cardio-renal syndrome model mice

Project description:The precise physiological mechanisms of cardio-renal syndrome are yet to be elucidated. In order to investigate the molecular basis of cardio-renal syndrome, we established a mouse model for cardio-renal syndrome by the combination of abdominal aortic banding and uninephrectomy. Renal function of the cardio-renal syndrome mice was synergistically decreased compared with that of mice that underwent uninephrectomy alone. To investigate the molecules involved in the deterioration renal function in the AbNx mice, we conducted comprehensive gene expression analysis using DNA array by comparing the molecules expressed in the remained kidney of AbNx mice with those of Nx mice. We conducted abdominal aorta banding or sham operation at 0 week, then We conducted uninephrectomy or sham operation at 2 week. We removed these kidney 6week after the uninephrectomy. These RNA samples were purified from the homogenized kidneys.

2012-03-19 | E-GEOD-36591 | biostudies-arrayexpress

Expression data from mouse kidney tissue

Project description:The role of the renin-angiotensin system in chronic kidney disease involves multiple peptides and receptors. Exerting antipodal pathophysiological mechanisms, renin inhibition and AT1 antagonism ameliorate renal damage. This is a comparison between the renin inhibitor aliskiren with the At1 antagonist losartan in mice with chronic kidney disease due to renal ablation. Renal tissue from ablated mice was used after 6-week treatment with either 500 mg/l losartan or 50 mg/kg aliskiren per day (n = 5)

2012-11-05 | E-GEOD-34552 | biostudies-arrayexpress

Expression data from renal dendritic cells under homeostatic conditions and from donor and host dendritic cells from renal allografts (3 days post-transplantation), isolated from cortex and medulla.

Project description:Renal dendritic cells play key roles in renal homeostasis and during kidney allograft rejection. Microarray analysis aims to evaluate whether dendritic cells modulate their gene expression profile in relation to their distribution in the different renal compartments (with varying biophysical characteristics), under homeostatic conditions and during acute renal allograft rejection (3 days post-transplantation). Renal dendritic cells from homeostatic (healthy) kidneys and donor/host dendritic cells from renal allografts (3 days post-kidney transplantation) were isolated from cortex and medulla, through fluorescence-activated cell sorting (FACS). Total RNA was isolated from FACS-sorted cells and amplified. The cDNA product was fragmented, biotin-labeled and hybridized on Affimetrix arrays.

2015-02-04 | E-GEOD-65564 | biostudies-arrayexpress

rat kidney LC-MS - Exploring the Therapeutic Mechanism of Desmodium styracifolium on Oxalate Crystal-Induced Kidney Injuries Using Comprehensive Approaches Based on Proteomics and Network Pharmacology

Project description:Oxalate-induced kidney injury rat model were established.The differentially expressed proteins in the kidneys between the oxalate and control groups were explored.

2018-10-19 | PXD009496 | Pride

Mouse kidney cisplatin TAILS - The proteome microenvironment determines the protective effect of preconditioning in cisplatin-induced acute kidney injury

Project description:Profiling of proteolytic events mouse kidneys during cisplatin-induced kidney damage. Kidneys from vehicle-treated mice are compared to cisplatin-treated mice and cisplatin treatment in animals preconditioned by hypoxia or calory restriction regimes.

2018-10-29 | PXD007186 | Pride

Analysis of the mouse kidney cortex phosphoproteome of VPS34 knockout and control animals

Project description:We generated phosphoproteomics data of renal cortices of mice with and without tubule-specific vps34 knockout.

2024-01-26 | PXD007093 | Pride

Major Action of Endogenous Lysyl Oxidase in Clear Cell Renal Cell Carcinoma Progression and Collagen Stiffness Revealed by Primary Cell Cultures

Project description:In this work we aimed to perform, for the first time in human clear cell renal cell carcinoma (ccRCC), a comprehensive and detailed study of endogenous LOX expression and functions. To overcome the difficulties and limitations due to tissue heterogeneity, we took advantage of a consolidated in vitro model of primary cell cultures that we obtained from normal kidney and ccRCC tissues. We have previously extensively characterized these primary cell cultures for their proteomic, cellular, and genomic features, and we also investigated here for their transcriptomic profile by using Affymetrix technology. This in vitro model has been instrumental for the molecular and functional analysis of endogenous LOX related to ccRCC progression.

2016-06-06 | E-MTAB-4074 | biostudies-arrayexpress

Microarray expression of kidney cortex in adult male rats treated with methylglyoxal vs. controls

Project description:In our study, we investigated the effect of methylglyoxal on metabolic, transcriptomic, metabolomic and proteomic profiles in the context of the development of kidney impairment in an experimental model of metabolic syndrome. Dicarbonyl stress was induced in experimental group by intragastrical administration of methylglyoxal (3x/ week in dose 0.5 mg/kg b.wt.for 4 weeks) in a strain of hereditary hypertriglyceridaemic rats (HHTg). Transcriptome assessment in kidney cortex was performed in 8 male adult rats of experimental group and compared to that of 6 age- and sex- matched rats of control group.

2020-02-08 | E-MTAB-7690 | biostudies-arrayexpress

TIMP2 and TIMP3 have divergent roles in early renal tubulointerstitial injury

Project description:Tissue inhibitors of metalloproteinases (TIMP) are endogenous inhibitors of matrix metalloproteinases (MMP). While TIMP2 and TIMP3 inhibit MMPs, TIMP3 also inhibits activation of pro-MMP2 whereas TIMP2 promotes it. Here we assessed the differential role of TIMP2 and TIMP3 in renal injury using the unilateral ureteral obstruction model. Gene microarray assay showed that post-obstruction, the lack of TIMP3 had a greater impact on gene expression of intermediate, late injury- and repair-induced transcripts, kidney selective transcripts and solute carriers. Renal injury in TIMP3-/-, but not in TIMP2-/- mice increased expression of collagen type I/III, connective tissue growth factor, transforming growth factor-Î² and the downstream Smad2/3 pathway. Interestingly, ureteral obstruction markedly increased MMP2 activation in the kidneys of TIMP3-/- mice which was completely blocked in the kidneys of TIMP2-/- mice. These changes are consistent with enhanced renal tubulointerstitial fibrosis in TIMP3-/- and its reduction in TIMP2-/- mice. The activity of tumor necrosis factor-Î± converting enzyme, caspase-3 and mitogen activated kinases were elevated in the kidneys of TIMP3-/- but not TIMP2-/- mice, suggesting enhanced activation of apoptotic and pathological signaling pathways only in the obstructed kidney of TIMP3-/- mice. Thus, TIMP2 and TIMP3 play differential and contrasting roles in renal injury, TIMP3 protects from damage whereas TIMP2 promotes injury through MMP2 activation. Kidneys from the wild type (WT), TIMP2-/- and TIMP3-/- mice undergoing sham or unilateral ureteral obstruction (UUO) procedures

2013-07-01 | E-GEOD-42303 | biostudies-arrayexpress

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