Mouse gut metagenome
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Project description:Renal failure is associated with accumulation of various solutes called Uremic toxins. Post transcriptional regulation related to Chronic kidney disease (CKD) have already been described as RNA based silencing with micro RNA or modifications of mRNA degradation. Until now, alternative splice modification was not mentioned in the course of CKD. However, CKD is associated with modification of gene expression. The aim of the study was to explore modification of the alternative splice pattern in the course in CKD. The expression level of individual exons expression in human fibroblast were compared after culture to 96 hours of uremic condition or control condition. Three independant experiments were performed
2013-08-16 | E-GEOD-41030 | biostudies-arrayexpress
Project description:Transcriptome analysis of human coronary arterial endothelial cells (HCAEC) primary cultures exposed to uremic serum from patients with stage 4-5 cardiovascular diseases (CKD) without myocardial infarction (USI) and stage 4-5 CKD with myocardial infarction (UCI). Gene expression profile of human coronary arterial endothelial cells (HCAEC) primary cultures exposed to uremic serum from of patients with chronic kidney disease (CKD) that explore which pathways are involved in in the development of cardiovascular disease. The metabolic pathway significantly represented was the MAPK signaling pathway, suggesting that the effects of uremic toxins present in patients with CDK, on the primary cultures of HCAEC provides a more informative model for the study of molecular mechanisms that lead to the development of endothelial dysfunction secondary to CKD.
2019-01-31 | GSE125898 | GEO
Project description:Background. Chronic renal failure is characterized by progressive renal scarring and accelerated cardiovascular disease. In animal models, this is thought to be due to non-dialyzable uremic toxins – small, protein-bound molecules normally secreted via Organic Anion Transporters (OATs) in the proximal renal tubule,rather than filtered at the glomerulus. The best studied of these is indoxyl sulfate (IS). Methods. We examined global gene expression responses in cultured normal human renal tubular cells incubated with control plasma (n=5) or pre- and post-dialysis uremic plasma (n=10). Results. GeneSpring analysis of microarrays revealed significantly altered expression of 2016 genes. The expression of 537 genes “normalized” in post-dialysis plasma, suggesting removal of “low molecular weight uremic toxins” by dialysis. The expression of the majority of dysregulated genes (1479) was not normalized in post-dialysis plasma. These likely represent the effects of substances not effectively removed by dialysis (“protein-bound uremic toxins”). Addition of indoxyl sulfateto control plasma simulated most effects (81.1%) of uremic plasma, while the addition of probenecid, an OAT inhibitor, to uremic plasma reversed most changes in gene expression. Analysis of molecular programs with the Gene Set Enrichment Analysis and the DAVID database revealed patterns common to indoxyl sulfate-treated control plasma, pre-dialysis, and post-dialysis uremic plasma. These included increased cell cycle, pro-inflammatory, and pro-fibrotic molecular programs, particularly genes in the TGF-β pathway. Conclusion: These findings provide insight into the role of non-dialyzable, protein-bound uremic toxins in the pathogenesis of renal scarring and uremic vasculopathy. The GSEA patterns confirm that inflammatory and fibrotic programs are active.
2013-06-30 | GSE45709 | GEO
Project description:Renal failure is associated with accumulation of various solutes called Uremic toxins. Post transcriptional regulation related to Chronic kidney disease (CKD) have already been described as RNA based silencing with micro RNA or modifications of mRNA degradation. Until now, alternative splice modification was not mentioned in the course of CKD. However, CKD is associated with modification of gene expression. The aim of the study was to explore modification of the alternative splice pattern in the course in CKD.
2013-08-16 | GSE41030 | GEO
Project description:Background. Chronic renal failure is characterized by progressive renal scarring and accelerated cardiovascular disease. In animal models, this is thought to be due to non-dialyzable uremic toxins M-bM-^@M-^S small, protein-bound molecules normally secreted via Organic Anion Transporters (OATs) in the proximal renal tubule,rather than filtered at the glomerulus. The best studied of these is indoxyl sulfate (IS). Methods. We examined global gene expression responses in cultured normal human renal tubular cells incubated with control plasma (n=5) or pre- and post-dialysis uremic plasma (n=10). Results. GeneSpring analysis of microarrays revealed significantly altered expression of 2016 genes. The expression of 537 genes M-bM-^@M-^\normalizedM-bM-^@M-^] in post-dialysis plasma, suggesting removal of M-bM-^@M-^\low molecular weight uremic toxinsM-bM-^@M-^] by dialysis. The expression of the majority of dysregulated genes (1479) was not normalized in post-dialysis plasma. These likely represent the effects of substances not effectively removed by dialysis (M-bM-^@M-^\protein-bound uremic toxinsM-bM-^@M-^]). Addition of indoxyl sulfateto control plasma simulated most effects (81.1%) of uremic plasma, while the addition of probenecid, an OAT inhibitor, to uremic plasma reversed most changes in gene expression. Analysis of molecular programs with the Gene Set Enrichment Analysis and the DAVID database revealed patterns common to indoxyl sulfate-treated control plasma, pre-dialysis, and post-dialysis uremic plasma. These included increased cell cycle, pro-inflammatory, and pro-fibrotic molecular programs, particularly genes in the TGF-M-NM-2 pathway. Conclusion: These findings provide insight into the role of non-dialyzable, protein-bound uremic toxins in the pathogenesis of renal scarring and uremic vasculopathy. The GSEA patterns confirm that inflammatory and fibrotic programs are active. Transcriptomic remodeling in response to external stimulus RNA from non-immortalized cultured renal cortical cells incubated with plasma samples from 5 controls, 10 uremics pre-dialysis, 10 uremics post-dialysis, 5 controls with indoxyl sulfate added, 5 uremics pre-dialysis with probenecid added, 5 uremics post-dialysis with indoxyl sulfate added
2013-06-30 | E-GEOD-45709 | biostudies-arrayexpress
Project description:<p><strong>OBJECTIVE:</strong> Patients with renal failure suffer from symptoms caused by uraemic toxins, possibly of gut microbial origin, as deduced from studies in animals. The aim of the study is to characterise relationships between the intestinal microbiome composition, uraemic toxins and renal failure symptoms in human end-stage renal disease (ESRD).</p><p><strong>DESIGN:</strong> Characterisation of gut microbiome, serum and faecal metabolome and human phenotypes in a cohort of 223 patients with ESRD and 69 healthy controls. Multidimensional data integration to reveal links between these datasets and the use of chronic kidney disease (CKD) rodent models to test the effects of intestinal microbiome on toxin accumulation and disease severity.</p><p><strong>RESULTS:</strong> A group of microbial species enriched in ESRD correlates tightly to patient clinical variables and encode functions involved in toxin and secondary bile acids synthesis; the relative abundance of the microbial functions correlates with the serum or faecal concentrations of these metabolites. Microbiota from patients transplanted to renal injured germ-free mice or antibiotic-treated rats induce higher production of serum uraemic toxins and aggravated renal fibrosis and oxidative stress more than microbiota from controls. Two of the species, Eggerthella lenta and Fusobacterium nucleatum, increase uraemic toxins production and promote renal disease development in a CKD rat model. A probiotic Bifidobacterium animalis decreases abundance of these species, reduces levels of toxins and the severity of the disease in rats.</p><p><strong>CONCLUSION:</strong> Aberrant gut microbiota in patients with ESRD sculpts a detrimental metabolome aggravating clinical outcomes, suggesting that the gut microbiota will be a promising target for diminishing uraemic toxicity in those patients.</p>
2020-10-20 | MTBLS700 | MetaboLights
Project description:We assessed the change in hepatic transciptional pattern after treatment with SGLT-2 inhibitors canagliflozin in a mice model of diet-induced obesity. Pharmacologic inhibition of the renal sodium/glucose cotransporter-2 induces glycosuria and reduces glycemia. Given that SGLT2 inhibitors (SGLT2i) reduce mortality and CV risk in T2D, improved understanding of molecular mechanisms mediating these metabolic effects is required. Treatment of obese but nondiabetic mice with the SGLT2i canagliflozin (CANA) reduces adiposity, improves glucose tolerance despite reduced plasma insulin, increases plasma ketones, and improves plasma lipid profiles. We utilized an integrated transcriptomic-metabolomics approach to demonstrate that CANA modulates key nutrient-sensing pathways, with activation of AMPK and inhibition of mTOR, independent of insulin or glucagon sensitivity or signaling. Moreover, CANA induces transcriptional reprogramming to activate catabolic pathways, increase fatty acid oxidation, reduce hepatic steatosis and diacylglycerol content, and increase hepatic and plasma levels of FGF21. Taken together, these data demonstrate that SGLT-2 inhibition triggers a fasting-like transcriptional and metabolic paradigm.
2020-04-16 | GSE148702 | GEO
Project description:Uremic pruritus (UP) is one of the common symptoms in patients with uremia, and its etiology and mechanism have not been fully understood. In view of the high incidence of UP, finding the specific changed proteins in blood of UP patients will help revealing the potential biological mechanisms of UP and explore biomarkers. In this study, LC-MS/MS based data independent acquisition (DIA) mode was used to analyze the serum samples of 54 UP patients (DKD-UP, HN-UP and GN-UP, n=18 for each), 18 uremic patients without pruritus (Negative) and 18 CKD patients without pruritus (CKD).
2024-03-08 | PXD045336 | Pride
Project description:Aging-related alterations of murine intestinal microbiota
| PRJDB9487 | ENA
Project description:End-stage renal disease (ESRD) is the final stage of chronic kidney disease, which is increasingly prevalent worldwide and is associated with the progression of cardiovascular disease (CVD). Indoxyl sulfate (IS) and p-cresyl sulfate (PCS), major uremic toxins, are major risk factors involved in the pathology of CVD via adverse effects on endothelial cells and immune cells. Thus, transcriptomic overview of uremic toxin-mediated genes in immune cells of ESRD patients is critical, but not yet fully known. We investigated the alteration of gene expressions and biological pathways mediated by major uremic toxins, in ESRD patients monocytes, via microarray analysis. To explore uremic toxin-related transcriptional profiling in ESRD patient-derived monocytes, purified monocytes from healthy controls were treated with IS or PCS for 24 hr, followed by conducting microarray on these samples.
2020-07-30 | GSE155325 | GEO