Ontology highlight
ABSTRACT:
PROVIDER: PRJNA202982 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cyclodextrin protects podocytes in diabetic kidney disease [HumanHT-12 V4.0 array]
| PRJNA202985 | ENA
Project description:Cyclodextrin protects podocytes in diabetic kidney disease [HumanWG-6 v3.0 array]
| PRJNA202986 | ENA
Project description:Analysis of gene expression changes in differentiated human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). The hypothesis is that the three groups can be distinghed by their differential gene expression pattern. The results obtained revealed important information regarding differences in gene expression in human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). Human podocytes were contacted with the serum from patients with diabetes and kidney disease (DKD+) or without kidney disease (DKD-) and compared to normal human podocytes contacted with serum from patients without diabetes (C).
2013-07-11 | E-GEOD-46897 | biostudies-arrayexpress
Project description:Analysis of gene expression changes in differentiated human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). The hypothesis is that the three groups can be distinghed by their differential gene expression pattern. The results obtained revealed important information regarding differences in gene expression in human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). Human podocytes were contacted with the serum from patients with diabetes and kidney disease (DKD+) or without kidney disease (DKD-) and compared to normal human podocytes contacted with serum from patients without diabetes (C).
2013-07-13 | E-GEOD-46899 | biostudies-arrayexpress
Project description:Analysis of gene expression changes in differentiated human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). The hypothesis is that the three groups can be distinghed by their differential gene expression pattern. The results obtained revealed important information regarding differences in gene expression in human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C).
2013-07-13 | GSE46899 | GEO
Project description:Analysis of gene expression changes in differentiated human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). The hypothesis is that the three groups can be distinghed by their differential gene expression pattern. The results obtained revealed important information regarding differences in gene expression in human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C).
2013-07-11 | GSE46897 | GEO
Project description:Podocyte injury is a key driver of progression in diabetic kidney disease (DKD). Because podocytes are underrepresented in whole-kidney single-cell RNA sequencing datasets, we performed single-cell RNA sequencing of isolated glomeruli from diabetic db/db mice and control db/m mice to generate a glomerulus-focused transcriptomic dataset. Diabetic glomeruli showed reduced podocyte abundance and extensive transcriptional remodeling. Integration of this in vivo dataset with in vitro analyses of cultured human podocytes exposed to diabetic stimuli identified OPCML, ADM, NELL2, and DHRS3 as candidate genes associated with diabetic podocyte injury. These findings identify OPCML, ADM, and DHRS3 as novel mediators of podocyte injury and potential therapeutic targets for DKD.
2026-09-17 | GSE337566 | GEO
Project description:Podocyte injury is a key driver of progression in diabetic kidney disease (DKD). Because podocytes are underrepresented in whole-kidney single-cell RNA sequencing datasets, we performed single-cell RNA sequencing of isolated glomeruli from diabetic db/db mice and control db/m mice to generate a glomerulus-focused transcriptomic dataset. Diabetic glomeruli showed reduced podocyte abundance and extensive transcriptional remodeling. Integration of this in vivo dataset with in vitro analyses of cultured human podocytes exposed to diabetic stimuli identified OPCML, ADM, NELL2, and DHRS3 as candidate genes associated with diabetic podocyte injury. These findings identify OPCML, ADM, and DHRS3 as novel mediators of podocyte injury and potential therapeutic targets for DKD.
2026-09-17 | GSE337565 | GEO
Project description:Podocytes play a pivotal role in maintaining homeostasis of the glomerular filtration barrier. The underlying mechanism is unclear but podocyte loss represents a critical event that contributes to the development of diabetic kidney disease (DKD). Proteinase 3 (PR3) is a serine protease with selective high abundance in myeloid cells and pleiotropic effects on the regulation of innate immunity. Here, we demonstrate that PR3 abundance in the kidney was markedly increased, predominantly in podocytes, in a mouse model of DKD. Genetic ablation of PR3 significantly attenuated severe proteinuria, mesangial matrix expansion, and podocyte injury in diabetic mice. The present study aimed to investigate the role of PR3 in glomerular podocytes in DKD.
2025-12-10 | GSE220631 | GEO
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