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Alteration of renal gene expression affected by atypical chemokine receptor D6 knockout in diabetic OVE26 (OVE) mice

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE51205 | GEO | 2013/10/10

SECONDARY ACCESSION(S): PRJNA221592

REPOSITORIES: GEO

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Alteration of renal gene expression affected by atypical chemokine receptor D6 knockout in diabetic OVE26 (OVE) mice

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.

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Temporal Gene Expression Patterns in the skin of D6 null and wild type mice after inflammation with the chemical irritant TPA

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Project description:The chemokine decoy receptor D6 internalises and degrades inflammatory CC chemokines enabling resolution of inflammation. In D6 deficient mice (D6 KO), otherwise innocuous cutaneous inflammatory stimuli induce a grossly exaggerated inflammatory response that bears many similarities to human psoriasis. In the present study we have used transcriptomic approaches to define the molecular make up of this response. The result of such analysis highlights potential roles for a number of cytokines iniating and maintaining psoriasis like pathology. Most compellingly, we provide data indicating a key role for the type I interferon pathway in the emergence of this pathology Backskin of D6 null mice was painted with three successive applications of 50uM TPA (in acetone), 24 hours apart. Control (labelled as day 0 or untreated) were treated with acetone only. After the three successive applications of TPA, pathology was left to develop for 1, 2, 4 or 6 days and backskin was taken for microarray analysis at each of these time points. To identify differentially expressed genes, comparisons were made between D6 KO and WT mice at each time point (D6 KO vs WT mice at day 0, day 1, day 2, day 4 or day 6). Significantly differentially expressed genes (p<0.05 according to an unpaired t-test) and up or down regulated more than 3 fold were identified ay each time point and selected for further analysis.

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Expression data from OVE26 diabetic mouse kidney

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.

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