Single-Cell Analysis of Age-Related Changes in Leukocytes of Diabetic Mouse Hindpaws
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE247211 | GEO | 2024/03/27
REPOSITORIES: GEO
Similar Datasets
Project description:The type 2 diabetes medication, rosiglitazone, has come under scrutiny for possibly increasing the risk of cardiac disease and death. To investigate the effects of rosiglitazone on the diabetic heart, we performed cardiac transcriptional profiling of a murine model of type 2 diabetes, the C57BL/KLS-leprdb/leprdb (db/db) mouse. We compared cardiac gene expression profiles from three groups: untreated db/db mice (db-c), db/db mice after rosiglitazone treatment (db-t), and non-diabetic db/+ mice.
2012-03-29 | GSE36875 | GEO
Project description:The type 2 diabetes medication, rosiglitazone, has come under scrutiny for possibly increasing the risk of cardiac disease and death. To investigate the effects of rosiglitazone on the diabetic heart, we performed cardiac transcriptional profiling of a murine model of type 2 diabetes, the C57BL/KLS-leprdb/leprdb (db/db) mouse. We compared cardiac gene expression profiles from three groups: untreated db/db mice (db-c), db/db mice after rosiglitazone treatment (db-t), and non-diabetic db/+ mice. Mice were divided into three groups: Non-diabetic controls (db/+), untreated diabetic controls (db-c), and rosiglitazone-treated diabetic mice (db-t). Whole-heart RNA from five mice from each of the three groups after four months with or without treatment was used for microarray analysis.Universal Reference RNAs for mouse (Stratagene, La Jolla, CA) were purchased as microarray reference controls.
2012-03-28 | E-GEOD-36875 | 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. 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:Diabetes is associated with altered metabolism, but how altered metabolism contributes to the development of complications such as diabetic kidney disease is unknown. We used a systems approach with transcriptomics and mass spectrometry (MS)-based metabolomics to determine alterations in carbohydrate and lipid metabolism in kidney cortex tissue from 24-week-old BKS db/db diabetic mice and db/+ controls. Glomerular-deprived kidney cortex (kidney proximal tubule) gene expression was profiled and compared with metabolite data. Transcriptomic and metabolomic profiling demonstrated an increase in both glycolysis and fatty acid beta-oxidation,
2016-12-08 | GSE86300 | GEO
Project description:Diabetic cardiomyopathy (DCM) is one of the most serious complications of diabetes. Recent cardiology studies suggest that spermine has cardioprotective effect. Here, we used proteomics analyses to reveal the underlying research target in type 2 diabetic mouse model treated with spermine. Left ventricular tissue was excised from 9 mice (Control group, 3; T2D group（db/db mouse）, 3; T2D+SP group, 3) and analyzed. Quantitative analysis of the global proteome were detected using 4D label-free technique,and differentially expressed proteins (DEPs) were used to perform bioinformatic analyses.
2022-10-13 | PXD036364 | Pride
Project description:Diabetic kidney disease (DKD) and diabetic peripheral neuropathy (DPN) are common complications of type 1 (T1D) and type 2 (T2D) diabetes. However, the mechanisms underlying the development and progression of these complications are unclear. Thus, the goal of the current study was to use system biology approaches to examine DKD and DPN pathogenesis in T1D and T2D mouse models on the same genetic background. We optimized a streptozotocin-induced db/+ murine model of T1D and compared it to our established db/db T2D mouse model of the same C57BLKS/J background and confirmed both develop DKD and DPN. Transcriptomic data from glomeruli and sciatic nerve tissue from T1D and T2D mice were analyzed by self-organizing map and differential gene expression analysis followed by functional enrichment. Consistent with prior literature, pathways related to immune function and inflammation were dysregulated in both DKD and DPN in T1D and T2D mice. The gene-level analysis identified a high degree of concordance in DEGs in both DKD and DPN and across diabetes type, suggesting genetic background influences diabetic complications. These findings offer new insight as the influence of genetic background on DPN in mouse models has not been well defined. Collectively, these findings support the role of inflammation and genetic background in complications of both T1D and T2D.
2023-09-08 | GSE222776 | GEO
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:Severe angiopathy is a major driver for diabetes associated secondary complications. Knowledge on underlying mechanisms essential for advanced therapies to attenuate these pathologies is limited. Injection of ABCB5+ stromal precursors (SPs) at the edge of non-healing diabetic wounds in a murine db/db model, closely mirroring human type II diabetes, profoundly accelerates wound closure. Strikingly, enhanced angiogenesis was substantially enforced by the release of the ribonuclease angiogenin from ABCB5+ SPs. This compensates for the profoundly reduced angiogenin expression in non-treated murine and human chronic diabetic wounds. Silencing of angiogenin in ABCB5+ SPs prior to injection significantly reduced angiogenesis, reduced numbers of M2 macrophages and delayed wound closure in diabetic db/db mice implying an unprecedented key role for angiogenin in tissue regeneration in diabetes. These data hold significant promise for further refining SPs-based therapies of non-healing diabetic foot ulcers and other pathologies with impaired angiogenesis.
2021-08-12 | GSE181881 | GEO
Project description:Diabetes promotes pro-atherogenic and pro-inflammatory phenotype of VSMC associated with vascular complications. Emerging evidence shows that miRNAs play key roles in VSMC, but their role in diabetes induced effects is unclear. We profiled novel diabetes induced miRNAs in VSMC from diabetic mice and examined their role in VSMC dysfunction. High throughput small RNA-sequencing identified 135 differentially expressed miRNAs in VSMC from type 2 diabetic db/db mice (db/dbVSMC) versus non-diabetic db/+ mice. Several of these miRNA were known to regulate VSMC functions. We further focused on miR-504, because it was highly upregulated in db/dbVSMC, but its function in VSMC is unknown. We demonstrated that miR-504 and its host gene Fgf13 were upregulated in VSMC and in vivo in aortas from db/db mice. Bioinformatics analysis predicted that miR-504 targets, including a signaling adaptor Grb10 and a transcription factor Egr2, could regulate growth factor signaling. We experimentally verified that miR-504 targets Grb10 and Egr2, and it enhanced ERK1/2 activation, proliferation and migration in VSMC. Silencing Grb10 by small interfering RNA also enhanced ERK1/2 activation, inflammatory gene expression and migration. Whereas, Egr2 silencing downregulated anti-inflammatory SOCS1 and increased inflammatory genes. Furthermore, treatment with high-glucose and palmitic acid upregulated miR-504, inhibited Grb10 and enhanced inflammatory genes in VSMC. Diabetes mis-regulates expression of several miRNAs including miR-504 involved in VSMC functions. Changes in miRNAs are sustained in non-diabetic conditions suggesting involvement of miRNA dependent mechanisms in metabolic memory implicated in vascular complications. Targeting such mechanisms could offer novel therapies strategies.
2016-04-15 | GSE74521 | GEO