E-GEOD-20636
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA124855
DISEASE(S): Normal,Diabetes Mellitus
PROVIDER: E-GEOD-20636 | ExpressionAtlas | 2015-09-15
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-20636-analysis-methods.tsv | Tabular | |||
| E-GEOD-20636-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-20636-configuration.xml | Xml | |||
| E-GEOD-20636-configuration.xml.beforeQC | Xml | |||
| E-GEOD-20636-percentile-ranks.tsv | Tabular |
Items per page: 5 1 - 5 of 88 |
Similar Datasets
Project description:In early development of diabetic nephropathy (DN), pathogenesis remains largely unknown. We used RNA-sequencing to profile protein-coding and long non-coding RNA (lncRNA) gene transcriptome of mouse kidney proximal tubular cells during early stage of DN at various time points. Over 7000 protein-coding and lncRNA genes were differentially expressed, and most of them were time-specific. Nearly 40% of lncRNA genes overlapped with functional element signals using CHIP-Seq data from ENCODE database. Disease progression was characterized by lncRNA expression patterns, rather than protein-coding genes, indicating that the lncRNA genes are potential biomarkers for DN. For gene ontologies related to kidney, enrichment was observed in protein-coding genes co-expressed with neighboring lncRNA genes. Based on protein-coding and lncRNA gene profiles, clustering analysis reveals dynamic expression patterns for kidney, suggesting that they are highly correlated during disease progression. To evaluate translation of mouse model to human conditions, we experimentally validated orthologous genes in human cells in vitro diabetic model. In mouse model, most gene expression patterns were repeated in human cell lines. These results define dynamic transcriptome and novel functional roles for lncRNAs in diabetic kidney cells; these roles may result in lncRNA-based diagnosis and therapies for DN.
2017-09-01 | GSE95376 | GEO
Project description:Diabetes is associated with altered metabolism, but how altered metabolism contributes to the development of complications such as diabetic kidney disease is unknown. We used a systems approach with transcriptomics and mass spectrometry (MS)-based metabolomics to determine alterations in carbohydrate and lipid metabolism in kidney cortex tissue from 24-week-old BKS db/db diabetic mice and db/+ controls. Glomerular-deprived kidney cortex (kidney proximal tubule) gene expression was profiled and compared with metabolite data. Transcriptomic and metabolomic profiling demonstrated an increase in both glycolysis and fatty acid beta-oxidation,
2016-12-08 | GSE86300 | GEO
Project description:Kidney injury is a common complication of severe disease. Here, we report that injuries of the zebrafish embryonal kidney are rapidly repaired by a migratory response in 2-, but not in 1-day-old embryos. Gene expression profiles between these two developmental stages identify cxcl12a and myca as candidates involved in the repair process. Zebrafish embryos with cxcl12a, cxcr4b, or myca deficiency display repair abnormalities, confirming their role in response to injury. In mice with a kidney-specific knockout, Cxcl12 and Myc gene deletions suppress mitochondrial metabolism and glycolysis, and delay the recovery after ischemia/reperfusion injury. Probing these observations in zebrafish reveal that inhibition of glycolysis slows fast migrating cells and delays the repair after injury, but does not affect the slow cell movements during kidney development. Our findings demonstrate that Cxcl12 and Myc facilitate glycolysis to promote fast migratory responses during development and repair, and potentially also during tumor invasion and metastasis.
2018-10-11 | MTBLS723 | MetaboLights
Project description:Regulation of gene expression by GLIS3 during neonatal kidney development
| PRJNA1002245 | ENA
Project description:Diabetic nephropathy is a major cause of end-stage renal disease. Kidney podocytes play a central role in the pathogenesis of diabetic nephropathy. With their intercellular contacts they assemble part of the kidney filter. Many molecular mechanisms of the pathogenesis of diabetic nephropathy are not elucidated and targeted therapies are lacking. Nephron-specific TrkCknockout (TrkC-KO) and TrkC overexpressing mice exhibit features of diabetic nephropathy such as enlarged glomeruli with mesangial proliferation, basement membrane thickening, albuminuria and podocyte loss when aging. Insulin-like growth factor 1 receptor (Igf1R)- associated gene expression was regulated in TrkC-KO mice glomeruli by qPCR. Phosphoproteins associated with insulin, erb-b2 receptor tyrosine kinase (Erbb) and Toll-like receptor signaling were enriched in lysates of podocytes treated with the TrkC ligand neurotrophin-3(Nt-3) in a mass spectrometry analysis. Activation of TrkC by Nt-3 resulted in phosphorylation of the Igf1R on activating tyrosine residues in podocytes. Our results identify TrkC to be a potentially targetable mediator of diabetic nephropathy.
2021-09-10 | PXD017960 | Pride
Project description:Alteration of kidney morphogenesis in diabetic pregnancies is poorly described, especially changes in the extracellular matrix (ECM) and glomerular basement membrane (GBM during glomerulogenesis. Addressing the ECM proteome, or matrisome, in the mouse fetal kidney in a healthy and diabetic environment will improve understanding about the association between ECM changes in the kidney as potential reprogramming mechanisms of kidney differentiation in diabetic pregnancies. Therefore, to better understand ECM composition and remodelling in kidney developmental and appreciate the alterations associated to the maternal diabetes, this project aimed to define the matrisome in the mouse fetal kidney on embryonic day 19. For this, we used an ECM enrichment approach combined with high resolution label-free tandem mass spectrometry to define the matrisome in the fetal mouse kidney (healthy and hyperglycemic) to test the hypothesis that maternal diabetes influences ECM composition, assembly and, therefore, biology.
2021-10-13 | PXD025874 | Pride
Project description:Differential gene expression profiles during embryonic heart development in diabetic mice pregnancy
| PRJNA147589 | ENA
Project description:We investigated the gene expression profiles of RNA isolated from kidney glomeruli from aged, 25 week old type-2 diabetic (db/db) and non-diabetic mice.
2016-10-24 | GSE77717 | GEO
Project description:Mouse models have been widely used to understand kidney disease pathomechanisms and play an important role in drug discovery. However, these models have not been systematically analyzed and compared. We analyzed single-cell RNA sequencing data (36 samples) and bulk gene expression data (42 samples) from 18 commonly used mouse kidney disease models. We compared single-nucleus RNA sequencing data from a mouse diabetic kidney disease model with data from patients with diabetic kidney disease and healthy controls. We generated a uniformly processed mouse single-cell atlas containing information for nearly 300,000 cells, identifying all major kidney cell types and states. Our analysis revealed that changes in fractions of cell types are major drivers of differences in bulk gene expression. Although gene expression changes at the single-cell level were mostly model-specific, different disease models showed similar changes when compared at a pathway level. Tensor decomposition analysis highlighted the important changes in proximal tubule cells in disease states. Specifically, we identified important alterations in expression of metabolic and inflammation-associated pathways. The mouse diabetic kidney disease model and patients with diabetic kidney disease shared only a small number of conserved cell type-specific differentially expressed genes, but we observed pathway-level activation patterns conserved between mouse and human diabetic kidney disease samples. This study provides a comprehensive mouse kidney single-cell atlas and defines gene expression commonalities and differences in disease states in mice. The results highlight the key role of cell heterogeneity in driving changes in bulk gene expression and the limited overlap of single-cell gene expression changes between animal models and patients, but they also reveal consistent pathway-level changes.
2023-09-15 | GSE220493 | GEO
Project description:Although diabetic nephropathy (DN) is the most common cause for end-stage renal disease (ESRD) in western societies, its pathogenesis still remains largely unclear. A different gene pattern of diabetic and healthy kidney cells is one of the probable explanations. Numerous signaling pathways have emerged as important pathophysiological mechanisms for diabetes-induced renal injury. Glomerular cells, as podocytes or mesangial cells, are predominantly involved in the development of diabetic renal lesions. While a lot of gene assays concerning DN are performed with whole kidney or renal cortex tissue, we isolated glomeruli from BTBR ob/ob and wildtype mice at 4 different timepoints (4, 8, 16, 24 weeks) and performed a mRNA microarray to identify differentially expressed genes (DEGs). In contrast to many other diabetic mouse models, these homozygous ob/ob leptin-deficient mice do not only develop a severe type II diabetes, but also diabetic kidney injury with all the clinical and especially histologic features defining human DN. The identified DEGs in diabetic glomeruli were used to investigate biological processes and pathways enriched at different disease stages.
2017-12-10 | GSE106841 | GEO