Glomerular Transcriptome Profiling Comparing DBA/2 and C57BL/6 mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Vivek Bhalla
PROVIDER: E-GEOD-84663 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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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:Diabetic nephropathy (DN) is a leading cause of ESRD worldwide, but its molecular pathogenesis is not well-defined and there are no specific treatments. In humans, there is a strong genetic component determining susceptibility to DN. However, specific genes controlling DN susceptibility in humans have not been identified. Here we describe a new mouse model, combining type 1 diabetes with activation of the renin angiotensin system (RAS), which develops robust kidney disease with features resembling human DN: heavy albuminuria, hypertension and glomerulosclerosis. Additionally, there is a powerful effect of genetic background regulating susceptibility to nephropathy. The 129 strain is susceptible to kidney disease, whereas the C57BL/6 strain is resistant. To examine the molecular basis of this differential susceptibility, we analyzed the glomerular transcriptome of young mice with albuminuria but without detectable alterations in glomerular structure. We find dramatic difference in regulation of immune and inflammatory pathways with up-regulation of pro-inflammatory pathways in the susceptible (129) strain and coordinate down-regulation in the resistant (C57BL/6) strain, compared to their respective baselines. Many of these pathways were also up-regulated in a rat model and in humans with DN. Our studies suggest that genes controlling inflammatory responses, triggered by hyperglycemia and hypertension, may be critical early determinants of susceptibility to DN. The analysis was carried out on 2 strains of mice (129/SvEv and C57BL/6), each involving 2 genotypes (wild-type and RenTg/Ins2Akita mutations). Four replicates were used for each strain-genotype (with the exception of 129/SvEv wild-type mice, which had 3 replicates).
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Project description:Murine models have been valuable instruments in defining the pathogenesis of diabetic nephropathy (DN), but they only partially recapitulate disease manifestations of human DN, limiting their utility . In order to define the molecular similarities and differences between human and murine DN, we performed a cross-species comparison of glomerular transcriptional networks. Glomerular gene expression was profiled in patients with early type 2 DN and in three mouse models (streptozotocin DBA/2 mice, db/db C57BLKS, and eNOS-deficient C57BLKS db/db mice). Species-specific transcriptional networks were generated and compared with a novel network-matching algorithm. Three shared, human-mouse cross-species glomerular transcriptional networks containing 143 (Human-STZ), 97 (Human- db/db), and 162 (Human- eNOS-/- db/db) gene nodes were generated. Shared nodes across all networks reflected established pathogenic mechanisms of diabetic complications, such as elements of JAK-STAT and VEGFR signaling pathways . In addition, novel pathways not formally associated with DN and cross-species gene nodes and pathways unique to each of the human-mouse networks were discovered. The human-mouse shared glomerular transcriptional networks will assist DN researchers in the selection of mouse models most relevant to the human disease process of interest. Moreover, they will allow identification of new pathways shared between mice and humans. We used microarrays to analyze the transcriptome of three different diabetic mouse models Glomerular RNA was extracted using the RNeasy Mini Kit and processed for hybridization on Affymetrix GeneChip Mouse Genome 430 2.0 microarrays.
2012-12-10 | E-GEOD-33744 | biostudies-arrayexpress
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
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Project description:Diabetic nephropathy (DN) is a leading cause of ESRD worldwide, but its molecular pathogenesis is not well-defined and there are no specific treatments. In humans, there is a strong genetic component determining susceptibility to DN. However, specific genes controlling DN susceptibility in humans have not been identified. Here we describe a new mouse model, combining type 1 diabetes with activation of the renin angiotensin system (RAS), which develops robust kidney disease with features resembling human DN: heavy albuminuria, hypertension and glomerulosclerosis. Additionally, there is a powerful effect of genetic background regulating susceptibility to nephropathy. The 129 strain is susceptible to kidney disease, whereas the C57BL/6 strain is resistant. To examine the molecular basis of this differential susceptibility, we analyzed the glomerular transcriptome of young mice with albuminuria but without detectable alterations in glomerular structure . We find dramatic difference in regulation of immune and inflammatory pathways with up-regulation of pro-inflammatory pathways in the susceptible (129) strain and coordinate down-regulation in the resistant (C57BL/6) strain, compared to their respective baselines. Many of these pathways were also up-regulated in a rat model and in humans with DN. Our studies suggest that genes controlling inflammatory responses, triggered by hyperglycemia and hypertension, may be critical early determinants of susceptibility to DN.
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Project description:We aim to study the gene expression changes in glomeruli of DBA/2 mice with diabetic nephropathy with or without Esm-1 over-expression. We extract pure mice glomeruli, prepared total cDNA with random hexamers and performed RNAseq study to quantify transcriptome and identify differential expressed genes. With a sequencing depth of 20M, we detected 12934 genes in total. We found many interferon related genes shows differences between control and DM group, suggesting DBA/2 mice with diabetic nephropathy are driven by interferon related mechanisms. We found 41 genes show biologically meaningful differences between DM and Esm-1 + DM group, suggesting these genes are downstream targets of Esm-1 in mice.
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Project description:We used scRNA-seq to confirm the rich cellular interactions between podocytes and glomerular parietal epithelial cells in early diabetic nephropathy and to construct a global view of early diabetic nephropathy.
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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:Murine models have been valuable instruments in defining the pathogenesis of diabetic nephropathy (DN), but they only partially recapitulate disease manifestations of human DN, limiting their utility . In order to define the molecular similarities and differences between human and murine DN, we performed a cross-species comparison of glomerular transcriptional networks. Glomerular gene expression was profiled in patients with early type 2 DN and in three mouse models (streptozotocin DBA/2 mice, db/db C57BLKS, and eNOS-deficient C57BLKS db/db mice). Species-specific transcriptional networks were generated and compared with a novel network-matching algorithm. Three shared, human-mouse cross-species glomerular transcriptional networks containing 143 (Human-STZ), 97 (Human- db/db), and 162 (Human- eNOS-/- db/db) gene nodes were generated. Shared nodes across all networks reflected established pathogenic mechanisms of diabetic complications, such as elements of JAK-STAT and VEGFR signaling pathways . In addition, novel pathways not formally associated with DN and cross-species gene nodes and pathways unique to each of the human-mouse networks were discovered. The human-mouse shared glomerular transcriptional networks will assist DN researchers in the selection of mouse models most relevant to the human disease process of interest. Moreover, they will allow identification of new pathways shared between mice and humans. We used microarrays to analyze the transcriptome of three different diabetic mouse models
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