Project description:Diabetic kidney disease (DKD) is a significant clinical challenge, with an increasing prevalence. Our research identified that fibroblast growth factor 4 (FGF4) secreted by podocytes is a key factor in a mouse model of DKD. Given the importance of FGF4 in DKD-induced kidney injury, we performed gene expression analysis on kidney tissues. This analysis compared db/db model mice with those treated with recombinant FGF4 (rFGF4). The results showed that, compared to the db/db model group, db/db mice treated with long-term rFGF4 demonstrated significant improvements in renal function markers, such as serum urea nitrogen and urinary protein levels.Overall, our findings indicate that FGF4 is a critical regulatory factor in DKD-induced renal injury, providing evidence that it alleviates glomerular damage by inhibiting oxidative stress and apoptosis.
Project description:We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples. Affymetrix expression arrays were used to identify differentially regulated transcripts in 44 microdissected human kidney samples. Stringent statistical analysis using the Benjamini_Hochberg corrected 2-tailed t-test was used to identify differentially expressed transcripts in control and diseased glomeruli and tubuli. This Series includes DKD and control glomeruli samples.
Project description:We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples. Affymetrix expression arrays were used to identify differentially regulated transcripts in 44 microdissected human kidney samples. Stringent statistical analysis using the Benjamini_Hochberg corrected 2-tailed t-test was used to identify differentially expressed transcripts in control and diseased glomeruli and tubuli. This Series includes DKD and control tubuli samples.
Project description:This SuperSeries is composed of the following subset Series: GSE30528: Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Glomeruli vs. Control Glomeruli) GSE30529: Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Tubuli vs. Control Tubuli) GSE30566: Transcriptome Analysis of Human Diabetic Kidney Disease (Control Glomeruli vs. Control Tubuli) Refer to individual Series
Project description:Analysis of gene expression changes in differentiated human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). The hypothesis is that the three groups can be distinghed by their differential gene expression pattern. The results obtained revealed important information regarding differences in gene expression in human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). Human podocytes were contacted with the serum from patients with diabetes and kidney disease (DKD+) or without kidney disease (DKD-) and compared to normal human podocytes contacted with serum from patients without diabetes (C).
Project description:Analysis of gene expression changes in differentiated human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). The hypothesis is that the three groups can be distinghed by their differential gene expression pattern. The results obtained revealed important information regarding differences in gene expression in human podocytes treated with the serum from patients with (DKD+) or without (DKD-) diabetic kidney disease when compared to normal subjects (C). Human podocytes were contacted with the serum from patients with diabetes and kidney disease (DKD+) or without kidney disease (DKD-) and compared to normal human podocytes contacted with serum from patients without diabetes (C).
Project description:We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples.
Project description:We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples.
Project description:Diabetic kidney disease (DKD), a progressive kidney disease, is a major complication associated with diabetes and has become the leading cause of chronic kidney disease in China. Increasing evidences have demonstrated that lncRNAs play vital roles in kidney diseases, including DKD. To search for new ncRNAs involved in DKD, we performed gene expression profiling in the kidney tissues isolated from DKD patients and non-diabetic renal cancer patients undergoing surgical resection by RNA sequencing. And we identified 65 DEncRNAs (29 upregulated and 36 downregulated in DKD) and 171 DEmRNAs (72 upregulated and 99 downregulated in DKD).This study will provide insights into the prevent and treatment of DKD in the future.
Project description:Diabetic kidney disease (DKD), a common and devastating microvascular complication of diabetes, is the leading cause of end-stage renal disease (ESRD). Since mechanisms of kidney injury in DKD were largely unknown, we performed single-cell RNA sequencing (scRNA-seq) on human kidneys collected from 3 DKD and 3 normal samples using 10×Genomics. In our study, a total of 51315 cells were enrolled for analyses and nine kidney cell types and seven immune cell types were identified. The cell-type-specific changes in gene expression and signaling pathways of podocyte, mesangial cells, endothelial cells, proximal tubule and macrophages indicate abnormal regulation associated with inflammation, apoptosis, oxidative stress, extracelluar matrix accumulation, and immune activation. In particular, we show that podocytes and renal tubular epithelial cells have a tremendous capacity to regenerate, which is involved in the repairment of injury. And extracellular vesicles, an important mediator of intercellular communication, might play a vital role for this progress. Besides, we identified new candidate transcription factors responsible for the progression of DKD. We also revealed a M1-M2 hybrid pattern, in which M1 and M2 are coupled activation in macrophages of DKD. Furthermore, we demonstrated a complex intercellular interaction between kidney cells and kidney cells or kidney cells and immune cells. Thus, our study will further the understanding of DKD pathogenesis and provide novel therapeutic targets for its treatment in the future.