Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA318387 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:microRNA in chronic kidney disease (CKD)
2017-01-01 | GSE80247 | GEO
Project description:Genetic Study of CHronic Kidney DIsease (CKD)
| PRJNA543915 | ENA
Project description:Genetic Study of CHronic Kidney DIsease (CKD)
| PRJNA543914 | ENA
Project description:Chronic kidney disease (CKD) complicates cisplatin-based chemotherapy of cancer patients. Here we investigate microRNA (miRNA)-regulated transcriptomic activity to unveil biological processes associated with cisplatin-induced kidney injury. Implementing chimeric-eCLIP-seq approach to a mouse model for cisplatin-induced CKD, we identify direct pairs of miRNA and their target messenger RNA in the injured kidney. We find a dedicated transcriptomic program directed by a group of miRNAs that alter metabolic pathways centered on mitochondria in the injured kidneys. Specifically, cisplatin-induced miRNA, miR-429-3p suppresses the mitochondria pathway that catalyzes branched-chain amino acid (BCAA), eventually leading to lipid peroxidation-dependent cell death, called ferroptosis. Thus, the identification of miRNA-429-3p-mediated stimulation of ferroptosis suggests a therapeutic potential for BCAA pathway modulation in ameliorating CKD and cisplatin-associated nephrotoxicity.
2023-11-01 | GSE242807 | GEO
Project description:Chronic kidney disease (CKD) is a progressive condition characterized by sustained alterations in kidney structure and function. Long-term kidney fibrosis is marked by glomerulosclerosis, vascular sclerosis, and tubulointerstitial fibrosis. Therefore we investigated the therapeutic potential of BMSC-CM on RPTEC/TERT1 in a fibrotic environment. Using PAA gel platforms, we mimicked the stiffness typical of chronic kidney disease patients' kidneys.
2023-12-20 | GSE250271 | GEO
Project description:We aimed to identify urinary exosomal ncRNAs as novel biomarkers for diagnosis of Chronic Kidney Disease (CKD) for this, we examined 15 exosomal ncRNA profiles in urine samples from CKD patients from four different stages (I, II, III and IV) and compared them to 10 healthy controls. We identified a significant number of novel, differentially expressed ncRNAs in CKD patients compared to healthy, which might be employed as early diagnostic markers in CKD in the future.
2016-11-30 | E-MTAB-5152 | biostudies-arrayexpress
Project description:Controlling the progression of chronic kidney disease (CKD) at an early stage is critical for reducing disease severity. A cross-sectional study of chronic kidney disease (CKD) patients at all stages with S. stercoralis infection found that helminth infection caused gut dysbiosis, which may be involved in CKD progression. Because of the variation of gut microbiome results with helminth infection, the cross-sectional study of 16S rRNA sequencing, therefore, is insufficient to draw valid conclusions and correct the effects of S. stercoralis on the early stages of CKD. Combination with other omics approach is warrant to be better understand the disease.
2024-01-24 | PXD039656 | JPOST Repository
Project description:We studied a murine AVF in mice with chronic kidney disease (CKD).
2018-06-27 | GSE116268 | GEO
Project description:Epidemiological studies indicate that adverse intrauterine and postnatal environment has a long-lasting role in chronic kidney disease (CKD) development. Epigenetic information can represent a plausible carrier for mediating this programming effect. Here we demonstrate that genome-wide cytosine methylation patterns of healthy and CKD tubule samples obtained from patients show significant differences. Cytosine methylation changes showed high concordance (98%) with a large (n=87) replication dataset. We rarely observed differentially methylated regions (DMR) on promoters. Histone modification-based kidney specific genome-wide gene regulatory region annotation maps (promoters, enhancers, transcribed and repressed regions) were generated. DMRs mostly overlapped with putative enhancer regions and were enriched in consensus binding sequences for important renal transcription factors, indicating their importance in gene expression regulation. A core set of genes, including transforming growth factors and collagens, showed cytosine methylation changes correlating with downstream transcript levels. Our report raises the possibility that epigenetic dysregulation plays a role in CKD development via influencing core profibrotic pathways. We used microarrays to detail the differences of gene expression of human tubule epithelial cells between chronic kidney disease and normal. We sought to decrease the cell type heterogeneity of kidney tissues to increase the resolution of expression profiles. To that end, microdissected human kidney tissue from both chronic kidney disease patient and normal are used for RNA extraction and hybridization on Affymetrix microarrays.
2013-07-18 | E-GEOD-48944 | biostudies-arrayexpress
Project description:Epidemiological studies indicate that adverse intrauterine and postnatal environment has a long-lasting role in chronic kidney disease (CKD) development. Epigenetic information can represent a plausible carrier for mediating this "programming" effect. Here we demonstrate that genome-wide cytosine methylation patterns of healthy and CKD tubule samples obtained from patients show significant differences. We rarely observed differentially methylated regions (DMR) on promoters. Histone modification-based kidney specific genome-wide gene regulatory region annotation maps (promoters, enhancers, transcribed and repressed regions) were generated. DMRs mostly overlapped with putative enhancer regions and were enriched in consensus binding sequences for important renal transcription factors, indicating their importance in gene expression regulation. A core set of genes, including transforming growth factors and collagens, showed cytosine methylation changes correlating with downstream transcript levels. Our report raises the possibility that epigenetic dysregulation plays a role in CKD development via influencing core profibrotic pathways. HG18_HELP array We used custom-commercial array to detail the differences of methylation regions of human tubule epithelial cells between chronic kidney disease and normal. We sought to decrease the cell type heterogeneity of kidney tissues to increase the resolution of methylation profiles. To that end, microdissected human kidney tissue from both chronic kidney disease patient and normal are used for the HELP-assay (HpaII tiny fragment Enrichment by Ligation-mediated PCR) and hybridization on Roche NimbleGen microarrays.
2013-08-09 | E-GEOD-49557 | biostudies-arrayexpress