Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1026807 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26346116.fastq.gz | Fastqsanger.gz | |||
| SRR26346117.fastq.gz | Fastqsanger.gz | |||
| SRR26346118.fastq.gz | Fastqsanger.gz | |||
| SRR26346119.fastq.gz | Fastqsanger.gz | |||
| SRR26346120.fastq.gz | Fastqsanger.gz |
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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: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: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: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:Chronic kidney disease (CKD), defined as a glomerular filtration rate <60 mL/min/1.73 m2 for at least 3 months, is a major public health concern with high prevalence in developed countries. CKD patients present dysregulations in their coagulation system, with higher levels of factor VII, factor VIII, thrombin, and tissue factor (main initiator of blood coagulation in vivo). Paradoxically, these patients present both an increased risk of thrombotic events and a higher bleeding rate compared to healthy subjects. Traditional cardiovascular risk factors are insufficient to explain the elevated rates of CVD, since it is the leading cause of death among CKD patients, rising uremic toxins as a possible link. Uremic toxins are compounds eliminated by the kidneys in physiological conditions. They tend to accumulate in the blood and tissues of patients with CKD due to its inadequate renal clearance. Uremia could influence biotransformation and transport across cellular membranes, disturbing drug tissue distribution. Therefore, CKD not only alters the elimination of drugs excreted by the kidneys, but it also impacts the metabolism of drugs subject to non-renal clearance, which involves mainly the liver and the gut. The liver is a highly specialized tissue, involved in the synthesis of plasma proteins and production of clotting factors, it has a major role in drug metabolization. The liver is also the main producer of thrombopoietin (hormone that regulates the production of platelets). All these processes are thought to be highly disturbed in CKD patients. Hepatocytes express high levels of AhR, ligand-inducible transcription factor activated by by xeno- and endobiotics, that mediate the induction of various liver cytochrome P450 enzymes. Hence, liver AhR regulates both nutrient metabolism and xenobiotic detoxification. Tryptophan derived uremic toxins (TDUT), induce tissue factor expression via the aryl hydrocarbon receptor (AhR) pathway, explaining the connection between CKD uremic toxin accumulation and hemostatic disbalances. Indoxyl sulfate (IS) is the main TDUT involved in uremic syndrome and acts as an AhR agonist in human primary hepatocytes. Tryptophan is metabolize to indole in the gut, absorbed into blood circulation and further process by the liver creating IS. In patients with CKD, IS tends to accumulate since it is poorly removed via dialysis. IS induces vascular endothelium and hemostatic dysfunction impacting cardiovascular morbidity and mortality during CKD. IS being a nephrotoxic, prothrombotic, pro-oxidative and pro-inflammatory molecule is proposed as the responsible for thrombotic events and metabolic changes in CKD patients. To further investigate the role of AhR and IS in metabolism and coagulation we want to analyse 60 C57BL/6J mice liver samples. These samples come from 8 different experimental groups: 4 groups of male mice and 4 groups of female mice. Each subset consists of a wildtype group treated with KCl (control), a KO AhR group treated with KCl (control), a wildtype group treated with 0,1% IS and a KO AhR group treated with 0,1% IS. The number of animals per group ranges from 6 to 8. Mice were fed ad libitum during the whole animal trial which started at 10 weeks of life. Both KCl and IS where solubilized in 5% sucrose water and administer in the drinking water of the mice for 1 week, after which mice were sacrificed at 11 weeks of age. KCl was used as control substance since IS is used under its potassium salt form. Although in many studies the variable gender is not considered, since we though that there could be a difference in basal expression as well as a hormonal bias that could influence the results, we decided to create separate experimental groups for both male and females. Hence, the large number of samples that needed to be analysed. The liver samples collected, were snap frozen and have been stored at −80 °C until further analyses.
2025-05-07 | PXD053404 | Pride
Project description:Cardiovascular disease (CVD) is exceedingly severe in patients with chronic kidney disease (CKD) and further aggravated by peritoneal dialysis (PD), exposing the patients to excessive amounts of intraperitoneal glucose. Children are devoid of pre-existing CVD and give insight into specific uremia and PD induced pathomechanisms. Fat surrounded omental arterioles beyond PD fluid penetration level were microdissected from uremic children at time of first PD catheter insertion (n=8), children on PD (n=5), and age and gender matched non-uremic children as controls (n=6). Adjacent sections of 4 arterioles per patient were used for transcriptomic analyses.
2018-04-12 | E-MTAB-5695 | biostudies-arrayexpress
Project description:Introduction: Cardiovascular pathology is the main cause of death in patients with chronic kidney disease (CKD). CKD is associated with the accumulation of uremic toxins in the bloodstream due to their difficult elimination by renal substitution therapy. Indoxyl sulfate (IS) is one of the most abundant uremic toxins found in the blood of patients with CKD. We conducted an in vitro study to assess the mechanisms underlying IS-induced endothelial dysfunction that could lead to cardiovascular diseases. We studied not only endothelial cells but also their extracellular vesicles (EVs) owing to their capacity to act as messengers that transmit signals through their cargo. Methods: EVs were characterized using nanoparticle tracking analysis, transmission electron microscopy, and flow cytometry, and their tetraspanin expression was evaluated to confirm their identity as EVs. Subsequently, mass spectrophotometry of the protein lysates of cells and EVs was performed, followed by Gene Set Enrichment Analysis to identify the principal altered pathways. Additionally, qPCR and proliferation analyses were performed to confirm proteomic results. Results: Proteomic analysis of endothelial cells revealed that IS causes an increase in proteins related to adipogenesis, inflammation, and xenobiotic metabolism and a decrease in proliferation via mTOR. Inflammation due to TNF signaling via NFкB was confirmed by an increase in the expression of the target genes IL-6, MCP-1, and ICAM-1. Concerning EVs, extracellular matrix elements were reduced, and myogenesis genes were downregulated in response to UV irradiation and inflammation. Fatty acid metabolism also seemingly increases, which, along with adipogenesis and inflammation observed in cells, could be related to atherosclerosis. Conclusions: Endothelial cells treated with IS had more proteins related to adipogenesis, inflammation, and xenobiotic metabolism and fewer associated with proliferation. Furthermore, EVs from cells treated with IS may mediate endothelial dysfunction, since they present fewer extracellular matrix elements, myogenesis and inflammatory factors, and proteins downregulated in response to UV radiation.
2024-11-29 | PXD050628 | Pride
Project description:Cardiovascular disease is highly prevalent in patients with chronic kidney disease (CKD) and responsible for approximately half of CKD-related deaths. The mechanisms underlying the detrimental impact of CKD on the heart are still incompletely understood, but CKD is associated with endocrinal, inflammatory and hemodynamic changes that impact the heart and may contribute to the development of uremic cardiomyopathy.
2025-01-17 | PXD050994 | Pride
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
Project description:Cardiovascular disease (CVD) is exceedingly severe in patients with chronic kidney disease (CKD) and further aggravated by peritoneal dialysis (PD), exposing the patients to excessive amounts of intraperitoneal glucose. Children are devoid of pre-existing CVD and give insight into specific uremia and PD induced pathomechanisms. Fat surrounded omental arterioles beyond PD fluid penetration level were microdissected from uremic children at time of first PD catheter insertion (n=8), children on PD (n=5), and age and gender matched non-uremic children as controls (n=6). Adjacent sections of 4 arterioles per patient were used for proteomic analyses.
2019-11-08 | PXD006298 | Pride