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E-GEOD-1009

ABSTRACT: Gene expression profiling in glomeruli from human kidneys with diabetic nephropathy

OTHER RELATED OMICS DATASETS IN: PRJNA87073

DISEASE(S): Normal,Diabetic Nephropathy

PROVIDER: E-GEOD-1009 | ExpressionAtlas | 2020-11-17

REPOSITORIES: ExpressionAtlas

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Dataset's files

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			Action	DRS
	E-GEOD-1009-analysis-methods.tsv	Tabular
	E-GEOD-1009-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-1009-configuration.xml	Xml
	E-GEOD-1009-percentile-ranks.tsv	Tabular
	E-GEOD-1009.condensed-sdrf.tsv	Tabular

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Diabetic nephropathy

Project description:Gene expression profiling in glomeruli from human kidneys with diabetic nephropathy Keywords = Diabetes Keywords = kidney Keywords = glomeruli Keywords: other

2004-04-01 | GSE1009 | GEO

Gene expression profiling in glomeruli from human kidneys with diabetic nephropathy

Project description:Gene expression profiling in glomeruli from human kidneys with diabetic nephropathy Keywords = Diabetes Keywords = kidney Keywords = glomeruli Keywords: other. This dataset is part of the TransQST collection.

2004-04-01 | E-GEOD-1009 | biostudies-arrayexpress

Single-cell profiling of glomerular cells provides a dynamic picture in experimental diabetic kidney disease

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

Expression data from kidneys of diabetic WT and T3-/- mice

Project description:Activation of A Disintegrin and A Metalloprotease Domain17 (ADAM17) is involved in nephropathy, but the role of this metalloprotease and its inhibitor TIMP3 in diabetic kidney disease is unclear. We used microarray profiling to find genes differentially expressed in the 2 genotypes which could explain the more severe diabetic kidney disease features observed in T3-/- mice compared to the WT littermates. Total RNA was extracted from 3 WT and 3 Timp3-/- diabetic kidneys

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Homo sapiens

Project description:Gene expression profiles of human kidneys

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Single-cell transcriptional profiles in glomeruli from type 2 db-/- mice

Project description:Diabetic nephropathy is a chronic complication of diabetes, presenting albuminuria at an early stage and leading to renal failure. Kidney is a complicated organ, which is responsible for body fluids control, acid-base balance, and removal of toxins. To better understand the progress of diabetic nephropathy, mice renal cortex of control mice, six-week db-/- (increased serum glucose without pathological changes in kidneys), and ten-week db-/- (with pathological changes in kidneys) were collected for single-cell sequencing analyses. A subgroup of glomerular endothelial cells with pro-angiogenetic features was identified in diabetic kidneys.

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Project description:There is a temporal window from the time diabetes is diagnosed to the appearance of overt kidney disease during which time the disease progresses quietly without detection. Currently, there is no way to detect early diabetic nephropathy (EDN). Here we performed an unbiased assessment of gene-expression analysis of postmortem human kidneys using microarrays to identify candidate genes that may contribute to EDN.

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Pomegranate Extract Supplementation in Colorectal Cancer Patients

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Differential microvascular endothelial cell responses in the retina in diabetes compared to the heart and kidneys, a spatial transcriptomic analysis.

Project description:Endothelial cells and high glucose-induced endothelial dysfunction are the common origin of chronic diabetic complications such as retinopathy, nephropathy, and cardiomyopathy. Yet their common origins, the vascular manifestations of such complications are different. We examined the basal heterogeneity between microvascular endothelial cells (MECs) from the retina, kidneys, and heart, as well as their differential responses to hyperglycemia in diabetes. To this extent, we used a spatial transcriptomic approach to investigate gene expression differences across retinal, renal, and cardiac MECs in diabetic and non-diabetic mouse models. We further validated MEC heterogeneity in vitro using human retinal and cardiac MECs. We found that MECs from different target organs of major diabetic complications were transcriptomically distinct at the basal state and respond differently to hyperglycemia.

2024-09-30 | GSE263128 | GEO

Transcription factor c-Maf deletion improves streptozotocin-induced diabetic nephropathy by directly regulating Sglt2 and Glut2

Project description:The transcription factor c-Maf has been widely studied and has been reported to play a critical role in embryonic kidney development; however, the postnatal functions of c-Maf in adult kidneys remain unknown as c-Maf null C57BL/6J mice exhibit embryonic lethality. In this study, we investigated the role of c-Maf in adult mouse kidneys by comparing the phenotypes of tamoxifen (TAM)-inducible c-Maf knockout mice (c-Maf flox/flox; CAG-Cre-ERTM mice named “c-Maf ΔTAM”) with that of c-Maf flox/flox control mice, 10 days after TAM injection (TAM(10d)). In addition, we examined the effects of c-Maf deletion on diabetic conditions by injecting the mice with streptozotocin (STZ), 4 weeks before TAM injection. c-Maf ΔTAM mice displayed primary glycosuria caused by Sglt2 and Glut2 downregulation in the kidneys without diabetes, as well as morphological changes and life-threatening injuries in the kidneys on TAM(10d). Under diabetic conditions, c-Maf deletion promoted recovery from hyperglycemia and suppressed albuminuria and diabetic nephropathy by causing similar effects as did Sglt2 knockout and SGLT2 inhibitors. In addition to demonstrating the unique gene regulation of c-Maf, these findings highlight the renoprotective effects of c-Maf deficiency under diabetic conditions and suggest that c-Maf could be a novel therapeutic target gene for treating diabetic nephropathy.

2023-02-01 | GSE199916 | GEO

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