Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA221592 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The D6 receptor can bind and internalize inflammatory chemokines without activating intracellular pathways. D6 can reduce tissue inflammation, presumably by scavenging inflammatory chemokines. In diabetic kidney there is extensive inflammation but the possible role of the D6 receptor has never been tested. In this study, we included the renal gene expression dataset generated from whole kidney RNA extraction in diabetic mice with or without D6 gene knockout, their controls are age and sex matched D6 deficient or wild type mice on FVB background. These data are used to analyze the effects of D6 deletion on progression of diabetic nephropathy. D6 knockout mice were crossing with FVB stain to produce D6 knockout mice in FVB background (D6). Then D6 was crossed with diabetic mice (OVE) to produce D6 defficient diabetic mice (OVE-D6). These mice were followed up for albuminuria from 2 month old, and sacrificied at 6 months for gene expression and renal morphology analysis. 12 kidney samples (3 per group) were used in this gene array study.
2013-10-10 | E-GEOD-51205 | biostudies-arrayexpress
Project description:The D6 receptor can bind and internalize inflammatory chemokines without activating intracellular pathways. D6 can reduce tissue inflammation, presumably by scavenging inflammatory chemokines. In diabetic kidney there is extensive inflammation but the possible role of the D6 receptor has never been tested. In this study, we included the renal gene expression dataset generated from whole kidney RNA extraction in diabetic mice with or without D6 gene knockout, their controls are age and sex matched D6 deficient or wild type mice on FVB background. These data are used to analyze the effects of D6 deletion on progression of diabetic nephropathy.
2013-10-10 | GSE51205 | GEO
Project description:OVE26 mouse was chosen to study the progressive changes in renal gene expression because it displays the most advanced albuminuria mouse models that assembles advanced human diabetic nephropathy. OVE26 mice induce inflammatory gene expression changes consistent with advanced renal disease, associated with severe albuminuria and not reported in any other diabetic models. They provide the first opportunity in a model of diabetic nephropathy to assess the effect of induction of inflammatory proteins that have been implicated in renal injury.
2010-03-06 | GSE20636 | GEO
Project description:OVE26 mouse was chosen to study the progressive changes in renal gene expression because it displays the most advanced albuminuria mouse models that assembles advanced human diabetic nephropathy. OVE26 mice induce inflammatory gene expression changes consistent with advanced renal disease, associated with severe albuminuria and not reported in any other diabetic models. They provide the first opportunity in a model of diabetic nephropathy to assess the effect of induction of inflammatory proteins that have been implicated in renal injury. Microarray expression was performed on whole kidney from control and diabetic mice at 2, 4 and 8 months of age and validated by rtPCR, in situ hybridization or immunohistochemistry.
2010-04-06 | E-GEOD-20636 | biostudies-arrayexpress
Project description:Objective – Previous studies showed that genetic deletion or pharmacological blockade of the Receptor for Advanced Glycation Endproducts (RAGE) prevents the early structural changes in the glomerulus associated with diabetic nephropathy (DN). To overcome limitations of mouse models that lack the progressive glomerulosclerosis observed in humans, we studied the contribution of RAGE to DN in the OVE26 type 1 mouse, a model of progressive glomerulosclerosis and decline of renal function. Research Design and Methods – We bred OVE26 mice with homozygous RAGE knock out (RKO) mice and examined structural changes associated with DN and used inulin clearance studies and albumin:creatinine measurements to assess renal function. Affymetrix Mouse 430.2 microarrays were used to measure the differential expression of OVE26vsFVB(WT) mice. Transcriptional changes in the TGF-?1 and Plasminogen activator inhibitor 1 gene products were measured by pcr to investigate mechanisms underlying accumulation of mesangial matrix in OVE26 mice. Results - Deletion of RAGE in OVE26 mice reduced nephromegaly, mesangial sclerosis, cast formation, glomerular basement membrane thickening, podocyte effacement, and albuminuria. The significant 29% reduction in glomerular filtration rate observed in OVE26 mice was completely prevented by deletion of RAGE. Increased transcription of the genes for Plasminogen activator inhibitor 1, TGF-?1, TGF-? induced, ?1- (IV) collagen observed in OVE26 renal cortex significantly reduced in OVE26 RKO kidney cortex. ROCK1 activity was significantly lower in OVE26 RKO compared to OVE26 kidney cortex. Conclusions - These data provide compelling evidence for critical roles for RAGE in the pathogenesis of DN and suggest that strategies targeting RAGE in long-term diabetes may prevent loss of renal function. The differential gene expression of OVE26 (diabetics) vs FVB (nodiabetic WT) mice was measured using Affymetrix Mouse 430.2 arrays.
2011-02-22 | E-GEOD-20844 | biostudies-arrayexpress
Project description:Objective – Previous studies showed that genetic deletion or pharmacological blockade of the Receptor for Advanced Glycation Endproducts (RAGE) prevents the early structural changes in the glomerulus associated with diabetic nephropathy (DN). To overcome limitations of mouse models that lack the progressive glomerulosclerosis observed in humans, we studied the contribution of RAGE to DN in the OVE26 type 1 mouse, a model of progressive glomerulosclerosis and decline of renal function. Research Design and Methods – We bred OVE26 mice with homozygous RAGE knock out (RKO) mice and examined structural changes associated with DN and used inulin clearance studies and albumin:creatinine measurements to assess renal function. Affymetrix Mouse 430.2 microarrays were used to measure the differential expression of OVE26vsFVB(WT) mice. Transcriptional changes in the TGF-β1 and Plasminogen activator inhibitor 1 gene products were measured by pcr to investigate mechanisms underlying accumulation of mesangial matrix in OVE26 mice. Results - Deletion of RAGE in OVE26 mice reduced nephromegaly, mesangial sclerosis, cast formation, glomerular basement membrane thickening, podocyte effacement, and albuminuria. The significant 29% reduction in glomerular filtration rate observed in OVE26 mice was completely prevented by deletion of RAGE. Increased transcription of the genes for Plasminogen activator inhibitor 1, TGF-β1, TGF-β induced, α1- (IV) collagen observed in OVE26 renal cortex significantly reduced in OVE26 RKO kidney cortex. ROCK1 activity was significantly lower in OVE26 RKO compared to OVE26 kidney cortex. Conclusions - These data provide compelling evidence for critical roles for RAGE in the pathogenesis of DN and suggest that strategies targeting RAGE in long-term diabetes may prevent loss of renal function.
2011-02-22 | GSE20844 | GEO
Project description:OVE26 (OVE) mice provide a useful model of advanced diabetic nephropathy (DN) with respect to albuminuria and pathologies. We showed that albuminuria, reduced GFR and interstitial fibrosis, which normally take 8-9 months to develop, are more advanced in uninephrectomized OVE mice within 10 weeks of surgery, at 4.5 months of age. The accelerated progression of renal damage, especially renal fibrosis in OVE-uni mice, was also identified at the gene expression level. The hepatic fibrosis/hepatic stellate cell activation pathway was by far the most significant Ingenuity canonical pathway identified by gene array in OVE-uni mice. Many inflammatory- and immune-related pathways were found among the top pathways up-regulated in OVE-uni kidneys, including acute-phase response signaling, leukocyte extravasation, IL6, IL10, IL12 signaling, TREM1 signaling, dendritic cell maturation and the complement system. These pathways were also dramatically up-regulated in 8-month-old OVE mice (GSE20636). Nephrectomized OVE mice are a much faster alternative model for studying advanced renal disease in diabetes. Study of renal gene expression in diabetic OVE26 mice. Uninephrectomy was used as an accelerating factor. Pooled RNA samples from 4 individual mice in each treatment group (OVE-uni, OVE-sham, FVB-uni, FVB-sham) were used for probe hybridization. Treatment groups: OVE-uni: uninephrectomy treatment in diabetic mice OVE-sham: sham surgery treatment in diabetic mice FVB-uni: uninephrectomy treatment in nondiabetic mice FVB-sham: sham surgery treatment in nondiabetic mice
2011-04-15 | E-GEOD-21448 | biostudies-arrayexpress
Project description:Renal gene expression in uninephrectomized diabetic OVE26 mice
| PRJNA126337 | ENA
Project description:Atypical chemokine receptor 1 controls haematopoiesis
| PRJNA341496 | ENA
Project description:Podocytes form filtration barrier through foot process around glomerualar basement membrane and selectively permit permeability of molecular smaller than albumin. Diabetes can cause podocyte pathological changes leading to high urine albumin level. Diabetic mouse model OVE26 has extremly high urine albumin and previously studies indicated its podocyte damaged. Here we try to find the key genes change in OVE26 diabetic mouse model podocyte by microarray assay while normal FVB mouse podocyte set as control. Podocyte eGFP transgenic mice were made on FVB background and crossbred to OVE26 diabetic model. Glomeruli isolated from OVE-GFP mice were digested by trypsin into signal cell. Podocytes with GFP were sorting out by FACS.
2012-03-02 | E-GEOD-36209 | biostudies-arrayexpress