Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA350859 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4471356_1.fastq.gz | Fastqsanger.gz | |||
| SRR4471356_2.fastq.gz | Fastqsanger.gz | |||
| SRR4471357_1.fastq.gz | Fastqsanger.gz | |||
| SRR4471357_2.fastq.gz | Fastqsanger.gz | |||
| SRR4471358_1.fastq.gz | Fastqsanger.gz |
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Project description:Single glomerular mesangial cells RNA-seq analysis
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Project description:Glomerular diseases are the leading cause of chronic kidney diseases with pathomechanisms largely unclear. It is known that ANGPT2 regulates endothelial cell homeostasis and function via TEK/TIE2 and its deregulation causes endothelial damage. We found that ANGPT2 is upregulated in glomerular diseases and wondered whether it has any effect on glomerular podocytes and mesangial cells given that they have no or low TEK expression. We treated podocytes and mesangial cells in culture with ANGPT2 and found no overt cellular changes. RNA-seq analysis showed that gene expression was altered in both podocytes and mesangial cells and that the regulated genes in the two cell types were fundamentally different. GO and KEGG analyses showed that the two groups of regulated genes were enriched in distinct processes and pathways. These results suggest that ANGPT2 exerts effects on both podocytes and mesangial cells and that increased ANGPT2 may be involved in glomerular injury by affecting podocytes and mesangial cells in addition to endothelial cells.
2022-01-10 | GSE185293 | GEO
Project description:Glomerular diseases are the leading cause of chronic kidney diseases with pathomechanisms largely unclear. It is known that ANGPT2 regulates endothelial cell homeostasis and function via TEK/TIE2 and its deregulation causes endothelial damage. We found that ANGPT2 is upregulated in glomerular diseases and wondered whether it has any effect on glomerular podocytes and mesangial cells given that they have no or low TEK expression. We treated podocytes and mesangial cells in culture with ANGPT2 and found no overt cellular changes. RNA-seq analysis showed that gene expression was altered in both podocytes and mesangial cells and that the regulated genes in the two cell types were fundamentally different. GO and KEGG analyses showed that the two groups of regulated genes were enriched in distinct processes and pathways. These results suggest that ANGPT2 exerts effects on both podocytes and mesangial cells and that increased ANGPT2 may be involved in glomerular injury by affecting podocytes and mesangial cells in addition to endothelial cells.
2022-01-10 | GSE185292 | GEO
Project description:To investigate dynamic changes in glomerular cells, including podocyte, mesangial cells and glomerular endothelial cells, in the development of diabetic nephropathy We then performed gene expression profiling analysis using data obtained from RNA-seq of glomerular cells of control(m/m), diabetic (db-/- 6-week-old) and diabetic nephropathy (db-/- 10-week-old with albuminuria) mice
2023-10-27 | GSE219268 | GEO
Project description:There are 3 cell types in a glomerulus: podocytes, mesangial cells and endothelial cells. These cell types play distinct roles in the structure and functions of glomeruli. In order to profile the gene expression of single glomerular cells, we isolated mouse glomeruli by Dynabead/magnetic concentration method and digested them with enzymes to dissociate them into single cells. We loaded the single cell suspension to a Fluidigm C1 Single-Cell Auto Prep System for single cell cDNA preparation. We performed qPCR analyses of marker genes of podocytes (Npsh2, Synaptopodin, WT1), mesangial cells (Gata3, IGFbp5) and endothelial cells (CD31, Tie2) to determine the identity of each cDNA sample. To identify podocyte-specific genes, we mixed 15 mesangial cell cDNA samples and 15 endothelial cell cDNA samples and further divided into 3 aliquots as replicates for sequencing using Illumina HiSeq 2000 system. The resulting data are used to compare with that of podocytes in order to identify podocyte-specific genes.
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2017-05-01 | GSE81055 | GEO
Project description:Renal blood filtration occurs in a functional unit called the glomerulus. The resident cell types comprise the filtration barrier, namely podocytes, mesangial cells and glomerular endothelial cells. Here we introduce a glomerular cell isolation protocol, which enables the separation of these three cell types in sufficient amounts and purity to allow detailed protein-biochemical investigations. We demonstrate that the expression of fluorescent transgenes in glomerular cells can result in proteome artifacts. We show that different mouse strains have different glomerular cell type proteomes. Further, we demonstrate the power of the technique to identify new glomerular cell type-enriched proteins and demonstrate the potential of this globally applicable technique in the dissection of cell-specific disease responses and intra-glomerular cell-type crosstalk.
2021-11-12 | PXD024481 | Pride
Project description:Background: Recent single-cell RNA sequencing (scRNA-seq) analyses have offered much insight into cell-specific gene expression profiles in normal kidneys. However, in diseased kidneys, understanding of changes in specific cells, particularly glomerular cells, remains limited. Methods: To elucidate the glomerular cell–specific gene expression changes in diabetic kidney disease, we performed scRNA-seq analysis of isolated glomerular cells from streptozotocin-induced diabetic endothelial nitric oxide synthase (eNOS)–deficient (eNOS-/-) mice and control eNOS-/- mice. Results: We identified five distinct cell populations, including glomerular endothelial cells, mesangial cells, podocytes, immune cells, and tubular cells. Using scRNA-seq analysis, we confirmed the expression of glomerular cell–specific markers and also identified several new potential markers of glomerular cells. The number of immune cells was significantly higher in diabetic glomeruli compared with control glomeruli, and further cluster analysis showed that these immune cells were predominantly macrophages. Analysis of differential gene expression in endothelial and mesangial cells of diabetic and control mice showed dynamic changes in the pattern of expressed genes, many of which are known to be involved in diabetic kidney disease. Moreover, gene expression analysis showed variable responses of individual cells to diabetic injury. Conclusion: Our findings demonstrate the ability of scRNA-seq analysis in isolated glomerular cells from diabetic and control mice to reveal dynamic changes in gene expression in diabetic kidneys, with variable responses of individual cells. Such changes, which might not be apparent in bulk transcriptomic analysis of glomerular cells, may help identify important pathophysiologic factors contributing to the progression of diabetic kidney disease.
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