Project description:Aim: To compare transcriptomic profiles of kidney cortex between healthy db/m mice, and mice with early stage diabetic kidney disease (uninephrectomized db/db injected with LacZAAV) and advanced stage diabetic kidney disease (uninephrectomized db/db mice injected with ReninAAV) Methods: Bulk RNA sequecing using the Illumina NextSeq 500 platform. Results: We identified 5,500 differentially expressed genes (DEGs) in db/db UNx LacZAVV mice compared to healthy controls, and 4,470 DEGs were identified in db/db UNx ReninAAV mice compared to healthy controls. Also, we showed in supplementery files that 3,039 DEGs were identified between db/db UNx LacZAAV mice and db/db UNx ReninAAV mice. Conclusion: We identified several gene expression changes in our two animal models of diabetic kidney disease.
2021-10-24 | GSE185616 | GEO
Project description:Single cell RNA sequencing of db/db mice kidney
| PRJNA749372 | ENA
Project description:scRNA-Seq of HKC treated db/db mice kidney
Project description:We have established a new fructose-overconsumption model using db/db mice, which showed more advanced kidney damage compared to the conventional db/db mouse model. To elucidate the mechanism of kidney injury caused by excessive fructose intake, we performed single-cell RNA analysis on the kidneys from this fructose-overconsumption model.
Project description:Dyslipidemia is a significant risk factor for progression of diabetic kidney disease (DKD). To identify individual lipids and lipid networks that may be involved in DKD progression, we performed untargeted lipidomic analysis of kidney cortex tissue from diabetic db/db and db/db eNOS-/- mice along with nondiabetic littermate controls. A subset of mice were treated with the renin-angiotensin system (RAS) inhibitors, lisinopril and losartan, which improves the DKD phenotype in the db/db eNOS-/- mouse model. Of the three independent variables in this study, diabetes had the largest impact on overall lipid levels in the kidney cortex, while eNOS expression and RAS inhibition had smaller impacts on kidney lipid levels. Kidney lipid network architecture, particularly of networks involving glycerolipids such as triacylglycerols, was substantially disrupted by worsening kidney disease in the db/db eNOS-/- mice compared to the db/db mice, a feature that was reversed with RAS inhibition. This was associated with decreased expression of the stearoyl-CoA desaturases, Scd1 and Scd2, with RAS inhibition. In addition to the known salutary effect of RAS inhibition on DKD progression, our results suggest a previously unrecognized role for RAS inhibition on the kidney triacylglycerol lipid metabolic network. Keywords: Dyslipidemia is a significant risk factor for progression of diabetic kidney disease (DKD). To identify individual lipids and lipid networks that may be involved in DKD progression, we performed untargeted lipidomic analysis of kidney cortex tissue from diabetic db/db and db/db eNOS-/- mice along with non-diabetic littermate controls. A subset of mice were treated with the renin-angiotensin system (RAS) inhibitors, lisinopril and losartan, which improves the DKD phenotype in the db/db eNOS-/- mouse model. Of the three independent variables in this study, diabetes had the largest impact on overall lipid levels in the kidney cortex, while eNOS expression and RAS inhibition had smaller impacts on kidney lipid levels. Kidney lipid network architecture, particularly of networks involving glycerolipids such as triacylglycerols, was substantially disrupted by worsening kidney disease in the db/db eNOS-/- mice compared to the db/db mice, a feature that was reversed with RAS inhibition. This was associated with decreased expression of the stearoyl-CoA desaturases, Scd1 and Scd2, with RAS inhibition. In addition to the known salutary effect of RAS inhibition on DKD progression, our results suggest a previously unrecognized role for RAS inhibition on the kidney triacylglycerol lipid metabolic network.
Project description:dB/dB mice develop different kidney pathologies resulting from high body weight. We seek to better understand the mechanisms of this kidney damage in proximal tubules. We isolated RNA from proximal tubules of different groups of mice, and we seek to understand how the anti-oxidant enzyme catalase may regulate kidney damage in this model.
Project description:db/db mouse kidney given liraglutide or insulin compared to db/db vehicle and healthy vehicle, 12 weeks dosing, all included db/db mice over 16 mM blood glucose level.
Project description:We investigated the gene expression profiles of RNA isolated from kidney glomeruli from aged, 25 week old type-2 diabetic (db/db) and non-diabetic mice. In order to investigate the consequences of hyperglycemia on the pathogenesis and progression of diabetic nephropathy Kidney glomeruli from 3 diabetic and 3 non-diabetic, control mice were isolated and RNA purified for RNA-Seq analysis on the Illumina HiSeq 2000. The goal of the project was to generate comprehensive list of noncoding RNA genes differentially regulated between the two conditions in order to identify novel targets for further study.
Project description:We investigated the gene expression profiles of RNA isolated from kidney glomeruli from aged, 25 week old type-2 diabetic (db/db) and non-diabetic mice.