Single-cell profiling of glomerular cells provides a dynamic picture in experimental diabetic kidney disease
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA524496 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8641420.fastq.gz | Fastqsanger.gz | |||
| SRR8641430.fastq.gz | Fastqsanger.gz | |||
| SRR8641440.fastq.gz | Fastqsanger.gz | |||
| SRR8641450.fastq.gz | Fastqsanger.gz | |||
| SRR8641460.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 1600 |
Similar Datasets
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.
2019-03-08 | GSE127235 | GEO
Project description:The objective of this study is to create an encyclopedia of all genes expressed in the glomerular endothelial cell under normal and diabetic conditions. We utilized Tie2-GFP transgenic mice to mark cells of the glomerular endothelium. To induce diabetic nephropathy (DB), a genetic model of DB, BKS.Cg-m +/+ Leprdb/J from Jax laboratories was used. We utilized fluorescent activated cell sorting (FACS) to isolate glomerular endothelial cells from normal and diabetic mice. The RNAs from these samples were isolated and utilized to hybridize to microarrays, which offers a powerful, efficient and effective method for the creation of a gene expression atlas. Microarrays were used to identify the transciptional differences that occur in the glomular endothelium of a diabetic mouse. Diabetic and control mice carrying the Tie2-GFP transgenic were utilized to isolate the endothelial cells from the adult glomerulus. The endothelial cells were isolated from the glomerulus using FACS. RNA was isolated and the gene expression profiles were determined by microarrays.
2010-08-16 | E-GEOD-21324 | biostudies-arrayexpress
Project description:The objective of this study is to create an encyclopedia of all genes expressed in the glomerular endothelial cell under normal and diabetic conditions. We utilized Tie2-GFP transgenic mice to mark cells of the glomerular endothelium. To induce diabetic nephropathy (DB), a genetic model of DB, BKS.Cg-m +/+ Leprdb/J from Jax laboratories was used. We utilized fluorescent activated cell sorting (FACS) to isolate glomerular endothelial cells from normal and diabetic mice. The RNAs from these samples were isolated and utilized to hybridize to microarrays, which offers a powerful, efficient and effective method for the creation of a gene expression atlas. Microarrays were used to identify the transciptional differences that occur in the glomular endothelium of a diabetic mouse.
2010-08-16 | GSE21324 | GEO
Project description:scRNA-seq analysis confirmed that increased LRG1 is limited to GECs in early diabetic kidneys. As anticipated, LRG1 loss significantly attenuated diabetic glomerulopathy including podocyte loss, and improved renal function. scRNA-seq analysis demonstrated that LRG1 loss was sufficient to reverse all significant molecular pathway changes in diabetic mouse GECs, which were also associated with the dampening of TGF-β-induced gene expression. Moreover, LRG1 loss also led to a significant attenuation of TGF-β-mediated gene expression in podocytes and mesangial cells of diabetic mice. These results indicate that increased LRG1 directly potentiates TGF-β signaling in glomerular cells in an autocrine and paracrine manner to promote DKD, and indirectly via glomerular cross-talk.
2024-12-26 | GSE269534 | GEO
Project description:Comparing glomerular gene expression level between mice with different susceptibilities to diabetic nephropathy, DBA/2 (susceptible) and C57BL/6 (resistant) mice, respectively. The hypothesis is that differential expression of glomerular genes regulate susceptibility to diabetic nephropathy. The results show immune related genes. Thus, glomerular inflammation may increase susceptibility to diabetic nephropathy in mice. RNA isolated from kidney glomeruli of DBA/2 and C57BL/6 mice, with or without 4 weeks diabetes induced by streptozotocin.
2016-07-22 | E-GEOD-84663 | biostudies-arrayexpress
Project description:Comparing glomerular gene expression level between mice with different susceptibilities to diabetic nephropathy, DBA/2 (susceptible) and C57BL/6 (resistant) mice, respectively. The hypothesis is that differential expression of glomerular genes regulate susceptibility to diabetic nephropathy. The results show immune related genes. Thus, glomerular inflammation may increase susceptibility to diabetic nephropathy in mice.
2016-07-22 | GSE84663 | 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:Set7 knockout (Set7KO) improved glomerular structure and albuminuria in a mouse model of diabetes. Analysis of mouse single-cell RNA-sequencing data showed dynamic transcriptional changes in diabetic renal cells. Set7KO controls phenotype switching of GEN cell populations through transcriptional regulation of the insulin growth factor binding protein 5 (IGFBP5). Chromatin immunoprecipitation assays confirmed that the expression of the IGFBP5 gene was associated with mono- and dimethylation of histone H3 lysine 4 (H3K4me1/2). This generalizability was investigated in human renal and circulating hyperglycemic cells exposed to TGFb1. We showed that the highly selective Set7 inhibitor PFI-2 attenuated indices associated with renal cell damage and mesenchymal transition, specifically (1) reactive oxygen species production, (2) IGFBP5 gene regulation, and (3) expression of mesenchymal markers. Furthermore, renal benefit observed in Set7KO diabetic mice closely corresponds in human glomerular endothelial cells with PFI-2 inhibition or Set7 shRNA silencing.
2024-04-17 | GSE158626 | GEO
Project description:Studies of diabetic glomerular injury raise the possibility of developing useful early biomarkers and therapeutic approaches for the treatment of type 2 diabetic nephropathy (T2DN). In this study, it is found that FGF13 expression is induced in glomerular endothelial cells (GECs) during T2DN progression, and endothelial-specific deletion of Fgf13 potentially alleviates T2DN damage. Fgf13 deficiency restores the expression of Parkin both in the cytosolic, mitochondrial, and nuclear fractions under diabetic conditions, resulting in improved mitochondrial homeostasis and endothelial barrier integrity due to promotion of mitophagy and inhibition of apoptosis. Additionally, it is confirmed that the beneficial effects of Fgf13 deficiency on T2DN are abolished by endothelial-specific double deletion of Fgf13 and Prkn. The effects of Fgf13 deficiency on mitophagy and apoptosis via Parkin-dependent regulation may be distinct and separable events under diabetic conditions. These data show that the bifunctional role of Fgf13 deficiency in promoting mitophagy and inhibiting apoptosis through Parkin can shape mitochondrial homeostasis regulation in GECs and T2DN progression. Acting as a potential biomarker and therapeutic target for prevention and control of T2DN, mechanistically understanding of the biofunction of FGF13 may also be of relevance to the pathogenesis of other FGF13- and Parkin-associated diseases.
2024-12-11 | GSE192889 | GEO
Project description:Albuminuria is significantly reduced following Roux-en-Y gastric bypass (RYGB) surgery, suggesting a renoprotective effect of the intervention. Herein, we assess the relative impact of RYGB and RYGB equivalent non-surgical weight loss and glycaemic improvement on glomerular injury and global renal transcriptomic responses in the Zucker diabetic fatty rat (ZDF) model of diabetic nephropathy. We coined the term "medical bypass" (MB) to describe the intensive diet and pharmacotherapy based non-surgical intervention Adult ZDF rats underwent sham surgery (n=15) or RYGB (n=9). Nine sham-operated rats were calorie restricted and received insulin, liraglutide, metformin, ramipril, rosuvastatin and fenofibrate for 2 months (MB). Zucker fa/+ rats acted as healthy controls throughout. Bodyweight, glycaemia, albuminuria and glomerular injury specifically podocyte number, density and ultrastructure were assessed at follow up. Renal transcriptomes were compared by RNA-seq. RYGB resulted in 20-30% weight loss, normalized glycaemia and albuminuria and reduced indices of glomerular injury, specifically podocyte injury (foot process effacement). RYGB equivalent outcomes were obtained on all parameters following MB.
2019-07-10 | GSE117378 | GEO