RNA-seq of iPSC-ECs treated with and without uremic toxin mixtures (UT-H).
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA656243 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR12421201_1.fastq.gz | Fastqsanger.gz | |||
| SRR12421201_2.fastq.gz | Fastqsanger.gz | |||
| SRR12421202_1.fastq.gz | Fastqsanger.gz | |||
| SRR12421202_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 11 |
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Project description:Three healthy iPSC lines were differentiated into ECs. iPSC-ECs were then treated with and without UT-H for 24 hours.
2021-02-02 | GSE155969 | GEO
Project description:Indoxyl sulfate (IS) is a uremic toxin and ligand of the aryl-hydrocarbon receptor (Ahr), a transcriptional regulator. Elevated serum IS may contribute to the progression of kidney disease. Therefore, we assessed mouse podocyte damage mediated by IS. Ahr was predominantly localized to the podocyte nucleus in vivo and in vitro. In isolated glomeruli, IS-exposure for 2 – 24 h induced Cyp1a1 expression, the most sensitive biomarker of Ahr activation. Mice exposed to IS for 4–8 weeks exhibited microalbuminuria, and mild glomerular injury characterized by ischemic changes, partial podocyte foot process effacement, as well as vascular and tubulointerstitial damage. Chronically IS-exposed kidneys exhibited decreased mRNA, decreased protein levels, and altered staining patterns for podocin, synaptopodin, and non-muscle myosin IIA (Myh9). Immortalized podocytes, upon differentiation, exhibited Ahr nuclear translocation beginning 30 min after 1 mM IS-exposure. At 2 h, there was a dose-dependent decrease in podocyte mRNA expression of WT1, Podxl, Snypo, Myh9, Actn4, and Cd2ap. After 24 h of exposure to IS, podocytes were smaller, had fewer actin/Myh9 fibers, and decreased viability. Ahr-RNAi decreased mRNA expression of podocyte-specific proteins and inhibited Cyp1a1 induction by IS-exposure. Combinations of Ahr-RNAi and IS-exposure further decreased Myh9 expression. In immortalized human podocytes, IS treatment caused cell injury, decreased mRNA expression of podocyte-specific proteins, integrins, collagens, cytoskeletal proteins, and bone morphogenetic proteins, and increased cytokine and chemokine expression. Thus, chronic IS-exposure causes glomerular damage by activating Ahr, altering podocyte function, differentiation, and morphology, and inducing a pro-inflammatory phenotype. Podocyte cells treated with Indoxyl sulfate, a uremic toxin and aryl-hydrocarbon receptor ligand, mediates progressive glomerular disease by damaging podocytes Human podocyte cell line treated with or without 3-Indoxyl sulfate (1mM/0.1%DMSO) in three replications
2014-10-14 | E-GEOD-51834 | biostudies-arrayexpress
Project description:Indoxyl sulfate (IS) is a uremic toxin and ligand of the aryl-hydrocarbon receptor (Ahr), a transcriptional regulator. Elevated serum IS may contribute to the progression of kidney disease. Therefore, we assessed mouse podocyte damage mediated by IS. Ahr was predominantly localized to the podocyte nucleus in vivo and in vitro. In isolated glomeruli, IS-exposure for 2 – 24 h induced Cyp1a1 expression, the most sensitive biomarker of Ahr activation. Mice exposed to IS for 4–8 weeks exhibited microalbuminuria, and mild glomerular injury characterized by ischemic changes, partial podocyte foot process effacement, as well as vascular and tubulointerstitial damage. Chronically IS-exposed kidneys exhibited decreased mRNA, decreased protein levels, and altered staining patterns for podocin, synaptopodin, and non-muscle myosin IIA (Myh9). Immortalized podocytes, upon differentiation, exhibited Ahr nuclear translocation beginning 30 min after 1 mM IS-exposure. At 2 h, there was a dose-dependent decrease in podocyte mRNA expression of WT1, Podxl, Snypo, Myh9, Actn4, and Cd2ap. After 24 h of exposure to IS, podocytes were smaller, had fewer actin/Myh9 fibers, and decreased viability. Ahr-RNAi decreased mRNA expression of podocyte-specific proteins and inhibited Cyp1a1 induction by IS-exposure. Combinations of Ahr-RNAi and IS-exposure further decreased Myh9 expression. In immortalized human podocytes, IS treatment caused cell injury, decreased mRNA expression of podocyte-specific proteins, integrins, collagens, cytoskeletal proteins, and bone morphogenetic proteins, and increased cytokine and chemokine expression. Thus, chronic IS-exposure causes glomerular damage by activating Ahr, altering podocyte function, differentiation, and morphology, and inducing a pro-inflammatory phenotype. Podocyte cells treated with Indoxyl sulfate, a uremic toxin and aryl-hydrocarbon receptor ligand, mediates progressive glomerular disease by damaging podocytes
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Project description:The urea channel Slc14a2 (or UT-A1) mediates vasopressin-regulated urea transport across the inner medullary collecting duct (IMCD). Previously, UT-A1 was found to present in a high molecular weight complex, suggesting UT-A1 is involved in certain protein-protein interactions. The present study sought to identify the proteins that interact with UT-A1 in this complex for a better understanding of how UT-A1 is regulated. Rat IMCD suspensions were treated with or without V2 receptor agonist, dDAVP, followed by in-cell crosslinking using BSOCOES and detergent solubilization. Immunoprecipitation using Dynabeads coated with UT-A1 specific antibody successfully pulled down the UT-A1 proteins. In-gel digestion protocol was carried out to prepare samples for liquid chromatographic mass spectrometry analysis of tryptic peptides using a Velos-Orbitrap mass spectrometer. The peptides passing stringent spectral quality thresholds were quantified (label-free) to identify those with (UTA-1 antibody/preimmune IgG) >4. A total of 128 UT-A1 interacting proteins were identified. Gene Ontology analysis maps the distribution of these proteins throughout major cell compartments: endoplasmic reticulum, Golgi, endosomes, cytosol and plasma membrane. Among them are four protein kinases (Cdc42bpb, Phkb, Camk2d, Mtor) that play roles in vasopressin-regulated phosphorylation of UT-A1. Non-label quantification was also performed to determine the stoichiometry of UT-A3 with UT-A1, the result does not support an oligomeric complex formation of UT-A1/A3. In conclusion, we have provided a refined list of UT-A1 binding proteins which can be useful for further analysis of the vasopressin signaling pathway in regulation of UT-A1 in IMCD.
2019-11-08 | PXD003496 | Pride
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:Adenine and nephrectomy can be used to establish models of uremic cardiomyopathy in rodents. Although these two approaches cause similar phenotypes of heart, adenine may directly act on cardiomyocytes and lead to different molecular changes from nephrectomy-induced uremic cardiomyopathy. Transcriptome analysis on left ventricles showed 789 upregulated and 345 downregulated genes in mice with nephrectomy-induced uremic cardiomyopathy compared to control mice, while 432 upregulated and 155 downregulated genes in mice with adenine diet-induced uremic cardiomyopathy compared to control mice. Functional analysis revealed that these DEGs were involved in pathways related to immune inflammation, metabolic responses, and synaptic transmission. Further analysis demonstrated that nephrectomy-induced uremic cardiomyopathy has enhanced cell cycle process/extracellular matrix remodeling and suppressed fatty acid metabolism, whereas adenine diet-induced uremic cardiomyopathy only exhibits increased inflammatory response/extracellular matrix remodeling. Compared with nephrectomy-induced uremic cardiomyopathy, adenine diet-induced uremic cardiomyopathy showed improved oxidative phosphorylation, aerobic electron transport chain, and tricarboxylic acid cycle, and suppressed cell cycle-related process, indicating that adenine and its derivates may affect the process of chronic kidney induced cardiac changes.
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Project description:In this study we mutated the ecsAB operon in two different Staphylococcus aureus strains, Newman and LS-1, and performed a wide characterization of phenotypic effects of the mutations. A growth defect, increased autolysis and lysostaphin sensitivity, decreased levels of cell wall proteins and altered cell surface texture indicate that Ecs deficiency causes significant changes in the cell wall. The precursor form of staphylokinase was released into the wall in an Ecs-dependent manner. Pathogenicity of the ecs mutants was studied with a mouse arthritis model. Mice inoculated with ecs mutants developed markedly milder infections than when inoculated with the wild-type strains, as was illustrated by a lower mortality, less weight loss, decreased persistence of staphylococci in the kidneys and a milder arthritis. DNA microarray analysis revealed that inactivation of Ecs in S. aureus Newman caused either up-regulation or down-regulation of genes encoding various membrane transport proteins, particularly ABC transporters and phosphate-specific transport (PST) systems. Differentially expressed were also several genes encoding proteins involved in virulence, including the virulence factor regulator protein Rot, protein A, adhesins and capsular polysaccharide biosynthesis proteins. Furthermore, the susceptibility of ecs mutant to ribosomal antibiotics as well as the chelerythrine and sanguinarine plant alkaloids was increased. WT and ecsA mutant strains were hybridized at 3 and 6 hours of growth in rich medium (4-replicates)
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Project description:Pachypodium lamerei isolate:UT Genome sequencing
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Project description:Shiga toxin type 2 (Stx2) is the main virulence factor produced by Stx-producing Escherichia coli (STEC) responsible for hemorrhagic colitis and the life-threatening sequela hemolytic uremic syndrome.
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Project description:Dynamic Gene Network Analysis of Caco-2 Cell Response to Shiga Toxin-Producing Escherichia coli-Associated Hemolytic–Uremic Syndrome
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