Gut Microbiome in Diabetic Nephropathy
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ABSTRACT:
PROVIDER: PRJEB36859 | ENA |
REPOSITORIES: ENA
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Project description:gut microbiome in diabetic nephropathy
| PRJEB36826 | ENA
Project description:Gene expression profiling in glomeruli from human kidneys with diabetic nephropathy Keywords = Diabetes Keywords = kidney Keywords = glomeruli Keywords: other
2004-04-01 | GSE1009 | GEO
Project description:Diabetic nephropathy (DN) is the leading cause of chronic kidney disease and end-stage renal disease. Emerging evidence suggests that complement activation is involved in the pathogenesis of DN. The aim of this study was to investigate the pathogenic role of C3a and C3a receptor (C3aR) in DN. The expression of C3aR was examined in the renal specimen of DN patients. Using a C3aR gene knockout mice (C3aR-/-), we evaluated kidney injury in diabetic mice. The mouse gene expression microarray was performed to further explore the pathogenic role of C3aR. Then the underlying mechanism was investigated in vitro with macrophage treated with C3a. Compared with normal controls, the renal expression of C3aR was significantly increased in DN patients. C3aR-/- diabetic mice developed less severe diabetic renal damage compared with WT diabetic mice, exhibiting significantly lower level of albuminuria and milder renal pathological injury. Microarray profiling uncovered significantly suppressed inflammatory responses and T cell adaptive immunity in C3aR-/- diabetic mice compared with WT diabetic mice and this result was further verified by immunohistochemical staining of renal CD4+, CD8+ T cells and macrophages infiltration. In vitro study demonstrated C3a can enhance macrophages secreted cytokines which could induce inflammatory responses and differentiation of T cell lineage. In conclusion, C3aR deficiency could attenuate diabetic renal damage through suppressing inflammatory responses and T cell adaptive immunity, possibly by influencing macrophages secreted cytokines. Thus, C3aR may be a promising therapeutic target for DN.
2020-04-10 | GSE133597 | GEO
Project description:Diabetic nephropathy (DN) is the leading cause of chronic kidney disease and end-stage renal disease. Emerging evidence suggests that complement activation is involved in the pathogenesis of DN. The aim of this study was to investigate the pathogenic role of C3a and C3a receptor (C3aR) in DN. The expression of C3aR was examined in the renal specimen of DN patients. Using a C3aR gene knockout mice (C3aR-/-), we evaluated kidney injury in diabetic mice. The mouse gene expression microarray was performed to further explore the pathogenic role of C3aR. Then the underlying mechanism was investigated in vitro with macrophage treated with C3a. Compared with normal controls, the renal expression of C3aR was significantly increased in DN patients. C3aR-/- diabetic mice developed less severe diabetic renal damage compared with WT diabetic mice, exhibiting significantly lower level of albuminuria and milder renal pathological injury. Microarray profiling uncovered significantly suppressed inflammatory responses and T cell adaptive immunity in C3aR-/- diabetic mice compared with WT diabetic mice and this result was further verified by immunohistochemical staining of renal CD4+, CD8+ T cells and macrophages infiltration. In vitro study demonstrated C3a can enhance macrophages secreted cytokines which could induce inflammatory responses and differentiation of T cell lineage. In conclusion, C3aR deficiency could attenuate diabetic renal damage through suppressing inflammatory responses and T cell adaptive immunity, possibly by influencing macrophages secreted cytokines. Thus, C3aR may be a promising therapeutic target for DN.
2020-04-10 | GSE133596 | GEO
Project description:Transcriptional profiling of human PBMCs comparing healthy controls, patients with diabetic nephropathy and patients with ESRD. PBMCs were analyzed as they mediate inflammatory injury. Goal was to determine effects of increasing severity of diabetic nephropathy on global PBMC gene expression. Microarray analysis of PBMCs taken from patients with varying degrees of diabetic nephropathy.
2020-12-01 | GSE142153 | GEO
Project description:Kidney structural integrity is critical for bodily excretory mechanism. Diabetes has been considered as one of the major risk factors for chronic kidney disease, but the underlying mechanism remains elusive. The present study investigates the transcriptomic and proteomic profiling of long-term impact of high-fat diet (HFD) on renal tissue in mice and role of dehydrozingerone (DH) in reinstating the normal kidney function. Animals were divided into four groups- healthy (NCD+Veh), diabetic (HFD-STZ+Veh), healthy+DH (NCD+Veh+DH) and treatment (HFD-STZ+DH). 65th days of HFD-fed C57BL/6 mice developed diabetes and kidney dysfunction evident by albuminuria, proteinuria, and glucotoxicity with accumulation of glucose, triglyceride, cholesterol, albumin, and total protein in blood serum. The HFD-fed kidney showed renal injuries, including prominent defects in the glomerular filtration system by downregulation of proteins involved in transport, metabolic process, energy production, anti-oxidation, etc. Downregulation of lipid metabolism is the most impacted metabolic process under diabetic condition. Downregulation of transport proteins mainly impact the functioning of podocytes, cell adhesion and cytoskeletal rearrangement. HFD feeding also increased oxidative stress and induced mitochondrial dysfunction, and thereby activating the pro-apoptotic pathway. Progression of DNA damage under diabetic condition triggered the epigenetic alteration and subsequent downstream changes which is evident by activation of HDAC1 under diseased condition. Transcriptomic study revealed the potential of dehydrozingerone in attenuating the diabetic condition by positively regulating transport system, mitochondrial function, lipid metabolism, DNA damage and epigenetic alteration, and oxidative stress, which ameliorate the kidney function.
2025-03-01 | GSE290410 | GEO
Project description:The present study aims to evaluate the alterations induced by type I diabetes and the associated hyperglycemia on the proteome of renal tissue using a transgenic experimental animal model. Diabetic and non-diabetic kidney samples were analyzed by liquid nano-chromatography mass spectrometry and protein abundance was evaluated bylabel free quantification.
2020-09-24 | PXD018053 | Pride
Project description:Background: Diabetic kidney disease (DKD) is a serious complication of diabetes mellitus and a leading cause of chronic kidney disease and end stage renal disease. One potential mechanism underlying cellular dysfunction contributing to kidney disease is aberrant post-translational modifications, such as lysine acetylation. Lysine acetylation is associated with cellular metabolic flux and is thought to be altered in patients with diabetes and dysfunctional renal metabolism. Methods: A novel technique was adapted to quantify sites of N-acetylation from formalin-fixed paraffin-embedded kidney explant tissue from patients with diabetic kidney disease and non-diseased donors (n=5 and n=7, respectively). Multiple methodologies were integrated to extract viable proteins from formalin-fixed paraffin-embedded kidney explant tissue followed by enrichment and isolation. Proteomic and acetylomic profiles were then quantified via LC-MS/MS analysis. Results: Quantitative proteomic analysis of FFPE tissues identified 840 total proteins with 260 of those significantly changing and our acetylomic analysis quantified 290 acetylated peptides with 98 of those significantly changing in human diabetic kidneys. Lysine acetylation is known to regulate protein function, providing a mechanism by which proteins respond to cellular metabolic status. Protein pathways found to be impacted in DKD patients revealed an association with numerous metabolic pathways, specifically mitochondrial function, EIF2 signaling, oxidative phosphorylation, lipid metabolism, sirtuin signaling, and LXR/RXR activation, each of which are intimated to play a significant role in the pathogenesis of DKD. Differential protein acetylation in DKD patients reflected biochemical processes associated with sirtuin signaling, valine, leucine, and isoleucine degradation, lactate metabolism, oxidative phosphorylation, and ketogenesis. Conclusions: Here, we establish a quantitative acetylomics platform for protein biomarker discovery in formalin-fixed and paraffin-embedded biopsies of kidney transplant patients suffering from diabetic kidney disease. Our analysis provides a novel platform for quantifying enriched post-translational modifications in preserved explant tissues and includes optimizations for addressing protein crosslinking, paraffin removal, and formalin-derived formaldehyde protein adducts combined with immunoprecipitation of acetyl-peptides and total protein quantitation.
2025-11-10 | PXD041884 | Pride
Project description:Diabetic nephropathy is a serious late chronic complication of type 2 diabetes and a major cause of end-stage renal disease. In order to better understand the molecular mechanisms of kidney lesions, we examined the mRNA and protein levels of mouse kidney to reveal the changes occurring in the kidney tissue of diabetes-associated kidney injury at the molecular level, to provide a theoretical basis for drug treatment.
2025-10-20 | PXD058790 | Pride
Project description:The effect of liraglutide on the kidney proteome in the STZ mouse model compared to healthy and STZ diabetic control groups.
2019-01-18 | PXD003007 | Pride