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: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.
Project description:We investigated the gene expression profiles of RNA isolated from kidney glomeruli and renal tubules from aged, 24 week old type-2 diabetic (db/db) and non-diabetic mice
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: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.
Project description:Purpose: Our study clarifies the mechanism of Huangqi decoction (HQD) against DKD in diabetic db/db mice. Methods: Eight-week-old male diabetic db/db mice were randomly divided into four groups: Model (1% CMC), HQD-L (0.12 g/kg), HQD-M (0.36 g/kg), and HQD-H (1.08 g/kg) groups. Non-diabetic db/m mice were used as a control group. These mice received HQD treatment for 8 weeks continuously. After 8 weeks of feeding, kidneys were harvested to observe the kidney function, pathological changes, micro-assay study, and the protein expression levels. Results: HQD treatment improved the albumin/creatine ratio (ACR) and 24 h urinary albumin, prevented the pathological phenotypes of increased glomerular volume, widened mesangial areas, the proliferation of mesangial matrix, the disappearance of foot processes, the decreased expression of nephrin and the number of podocytes. The expression profile chips were assessed to reveal the global transcriptional response and predict related functions, diseases and pathways. To verify this, we found that HQD treatment activated the protein expressions of BMP1, BMP7, BMPR2, and active-Rap1 and inhibited Smad1 and phospho-ERK. In addition, HQD could improve lipid deposition in the kidneys of db/db mice. Conclusion: HQD prevents the progression of DKD in db/db mice by regulating the transcription of BMPs and their downstream target genes, inhibiting the phosphorylation of ERK and Smad1 by promoting the binding of Rap1 to GTP and regulating the lipid metabolism dysfunction. These provide a new idea for the treatment of DKD. Overall, HQD had a significant protective effect against DKD. This may be related to the fact that HQD promotes the transcription of BMPs and their downstream target genes by upregulating BMPR-II and regulates the phosphorylation of ERK and Smad by promoting the binding of Rap1 to GTP. In addition, HQD also has a noticeable role in regulating lipid metabolism dysfunction in DKD, which provides a new idea for future research on HQD.
Project description:Diabetic nephropathy(DN) is a common diabetic microvascular complication, the underlying mechanisms involved in DN remain to be elucidated. We used microarrays to explore the global profile of gene expression for better understanding the molecular mechanism of diabetic nephropathy in type 2 diabetic db/db mice.