Bulk RNA-sequencing of FACS-sorted kidney glomerular cell types from BTBR ob/ob mice and glomeruli isolated from ex vivo perfused kidneys
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ABSTRACT:
PROVIDER: PRJNA902307 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22311600.fastq.gz | Fastqsanger.gz | |||
| SRR22311601.fastq.gz | Fastqsanger.gz | |||
| SRR22311602.fastq.gz | Fastqsanger.gz | |||
| SRR22311603.fastq.gz | Fastqsanger.gz | |||
| SRR22311604.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the gene expression levels of major glomerular cell types in BTBR ob/ob mice and in glomeruli under hyperfiltration Bulk RNA-sequencing of glomerular cell types from BTBR ob/ob and BTBR +/+ mice at three time points (6/12/18 weeks). The glomeruli were isolated from ex vivo perfused kidney (hyperfiltration) and unperfused kidney (control) from the mouse.
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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.
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Project description:Analysis of gene expression in glomeruli of BTBR ob/ob diabetic mice
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Project description:We found that 18-week administration of a prolyl hydroxylase inhibitor, enarodustat, improved glucose/lipid metabolism of BTBR ob/ob mice, which is a model of obesity and type 2 diabetes mellitus. Enarodustat-treated mice also exhibited reduced albuminuria along with ameliorated glomerular epithelial and endothelial damage. In order to elucidate the mechanism of renoprotection, we performed microarray gene expression analysis of isolated glomeruli. The initial screening process revealed 8965 probes whose absolute values of log2 (BTBR ob/ob mice treated with enarodustat/BTBR ob/ob mice treated with vehicle-only) exceeded 0.5. We then compared the expression levels of those 8965 probes between BTBR ob/ob and wild-type mice to identify molecules that were likely to be involved in the pathogenesis of glomerular injury. Such analysis revealed 71 genes which were significantly up-regulated and 47 genes which were significantly down-regulated in BTBR ob/ob mice compared to wild-type mice. The genes were ranked according to their fold-change values, and the analysis presented Ccl2/Mcp1 as the second-most up-regulated gene in BTBR ob/ob mice. The expression level of Ccl2/Mcp1 increased by 24.42-fold in BTBR ob/ob compared to wild-type mice, and its expression in enarodustat-treated BTBR ob/ob mice was decreased to 0.62 of the vehicle-only treated BTBR ob/ob mice. Urinary CCL2/MCP-1 was indeed decreased in enarodustat-treated BTBR ob/ob mice. In vitro experiments also showed that enarodustat suppressed palmitate-induced CCL2/MCP-1 production in murine mesangial cells. Taken together, enarodustat is likely to confer renoprotection through regulating the expression of CCL2/MCP-1 in the glomerulus.
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Project description:Female mouse models of diabetic peripheral neuropathy (DPN) have not yet been identified. Our aim is firstly to demonstrate that female BTBR ob/ob mice display robust DPN and secondly, to perform relevant comparisons with non-diabetic and gender-matched controls. Lastly, microarray technology was employed to identify dysregulated genes and pathways in the SCN and DRG of female BTBR mice. Dorsal root ganglia (DRG) and sciatic nerve (SCN) were removed from female mice, RNA isolated and processed for gene expression profiling to identify differentially expressed genes using Affymetrix GeneChip Mouse Genome 430 2.0 Arrays.
2016-07-12 | GSE70852 | GEO
Project description:The expression of adipogenic genes is decreased in obesity and diabetes mellitus ; Samuel T. Nadler*, Jonathan P. Stoehr*, Kathryn L. Schueler*, Gene Tanimoto, Brian S. Yandell, and Alan D. Attie*,§ ; Departments of * Biochemistry, and Statistics and Horticulture, University of Wisconsin, Madison, WI, 53706; and Affymetrix, Inc., Santa Clara, CA 95051 ; Communicated by Neal L. First, University of Wisconsin, Madison, WI, July 13, 2000 (received for review April 3, 2000) ; Obesity is strongly correlated with type 2 diabetes mellitus, a common disorder of glucose and lipid metabolism. Although adipocytes are critical in obesity, their role in diabetes has only recently been appreciated. We conducted studies by using DNA microarrays to identify differences in gene expression in adipose tissue from lean, obese, and obese-diabetic mice. The expression level of over 11,000 transcripts was analyzed, and 214 transcripts showed significant differences between lean and obese mice. Surprisingly, the expression of genes normally associated with adipocyte differentiation were down-regulated in obesity. Not all obese individuals will become diabetic; many remain normoglycemic despite profound obesity. Understanding the transition to obesity with concomitant diabetes will provide important clues to the pathogenesis of type 2 diabetes. Therefore, we examined the levels of gene expression in adipose tissue from five groups of obese mice with varying degrees of hyperglycemia, and we identified 88 genes whose expression strongly correlated with diabetes severity. This group included many genes that are known to be involved in signal transduction and energy metabolism as well as genes not previously examined in the context of diabetes. Our data show that a decrease in expression of genes normally involved in adipogenesis is associated with obesity, and we further identify genes important for subsequent development of type 2 diabetes mellitus. Experiment Overall Design: For obesity study, lean samples include C57BL/6J lean, (C57BL/6J X BTBR) F1 and BTBR lean, obese sampples incluse C57BL/6J-ob/ob, (C57BL/6J X BTBR) F2-ob/ob and BTBR-ob/ob. All samples are subjected to Mu11K A and B arrays. Experiment Overall Design: For diabetes study, B6-ob/ob, (C57BL/6J X BTBR) F2-ob/ob low glucose, (C57BL/6J X BTBR) F2-ob/ob medium glucose, (C57BL/6J X BTBR) F2-ob/ob high glucose, and BTBR-ob/ob samples were analyzed for genes whose expression levels changes correlated with the plasma glucose levels in these mice. All samples are subjected to Mu11K A and B arrays.
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Project description:The specific contribution of the two TNF-receptors Tnfr1 and Tnfr2 to TNF-induced inflammation in the glomerulus is unknown. In mice, TNF exposure induces glomerular expression of inflammatory mediators like adhesion molecules and chemokines in vivo, and glomerular accumulation of leukocytes. To examine Tnfr-specific inflammatory responses in intrinsic glomerular cells but not infiltrating leukocytes we performed microarray gene expression profiling on intact glomeruli isolated from wild-type and Tnfr-deficient mice following TNF exposure in vitro. Glomeruli were isolated from male C57BL/6J wild-type and Tnfr-deficient mice applying a magnetic bead-based isolation technique. Isolated intact glomeruli were stimulated with TNF for 12 hours in vitro for subsequent RNA extraction and hybridization on Affymetrix microarrays.
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Project description:We compared the gene expression analysis of 2 different glomerular isolation techniques (laser capture microdissection with 2 rounds of RNA amplification and unamplified glomerular RNA after iron perfusion with glomerular sieving) and obtained different results depending on the glomerular isolation technique that was used Experiment Overall Design: Paired kidneys from Lewis-Hsd rat kidneys were collected. The glomeruli of one kidney was obtained by LCM with 2 rounds of RNA amplification while the unamplified glomerular RNA of the contralateral kidney was obtained after perfusion with iron oxide and isolated by magnetic purification and a glomerular sieving technique. The RNA was analyzed using the Affymetrix Rat 230A microarrays.
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Project description:The specific contribution of the two TNF-receptors Tnfr1 and Tnfr2 to TNF-induced inflammation in the glomerulus is unknown. In mice, TNF exposure induces glomerular expression of inflammatory mediators like adhesion molecules and chemokines in vivo, and glomerular accumulation of leukocytes. To examine Tnfr-specific inflammatory responses in intrinsic glomerular cells but not infiltrating leukocytes we performed microarray gene expression profiling on intact glomeruli isolated from wild-type and Tnfr-deficient mice following TNF exposure in vitro.
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