Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA321466 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene Expression Profiles of Transplanted Kidneys from Deceased Donors with Severe Acute Kidney Injury
2025-01-24 | E-GEOD-61739 | ExpressionAtlas
Project description:Transcription profiling of molecular phenotypes of acute kidney injury in kidney transplants
2025-01-24 | E-GEOD-30718 | ExpressionAtlas
Project description:Contrast-induced acute kidney injury (CI-AKI) is typically defined by an increase in serum creatinine (SCr) after intravascular administration of contrast medium. Since creatinine is an unreliable indicator for acute changes in kidney function, an early biomarkers for CI-AKI diagnosis is important for initiating therapy.We assessed the hypothesis that circulating microRNAs (miRNAs) could be served as potential biomarkers to early detect CI-AKI.The rat model of acute kidney injury was developed as we previously described. We first detect miRNA profile of plasma and kidney tissue using Agilent microarray platform. 3 miRNA species with > 1.5-fold increase in plasma samples of CI-AKI rats, including miRNA-30a, miRNA-30e and miRNA-188, were selected as candidate miRNAs of potential biomarkers. 24 rats were randomly divided into 2 groups (CI-AKI group and control group), each with 4 subgroups (n=3). Peripheral blood and kidney samples were harvest at 8h after contrast medium/normal saline administration. Total RNA sample from each rat in the same subgroup was combined together as pooled sample for further test. The Agilent microarray platform was adapted to profile the miRNA spectra.
2016-05-14 | E-GEOD-81400 | biostudies-arrayexpress
Project description:Contrast-induced acute kidney injury (CI-AKI) is typically defined by an increase in serum creatinine (SCr) after intravascular administration of contrast medium. Since creatinine is an unreliable indicator for acute changes in kidney function, an early biomarkers for CI-AKI diagnosis is important for initiating therapy.We assessed the hypothesis that circulating microRNAs (miRNAs) could be served as potential biomarkers to early detect CI-AKI.The rat model of acute kidney injury was developed as we previously described. We first detect miRNA profile of plasma and kidney tissue using Agilent microarray platform. 3 miRNA species with > 1.5-fold increase in plasma samples of CI-AKI rats, including miRNA-30a, miRNA-30e and miRNA-188, were selected as candidate miRNAs of potential biomarkers.
2016-05-14 | GSE81400 | GEO
Project description:Entrapment Neuropathy Results in Different MicroRNAs Expression Patterns from Denervation Injury in Rats
| PRJNA128813 | ENA
Project description:Purpose:little is known about the roles of lncRNA in the pathogenesis of contrast-induced acute kidney injury (CI-AKI). Here, we compared the expression profiles of lncRNAs and mRNAs in kidney tissue between CI-AKI rats and controls. Methods:Based on a reliable CI-AKI rat model, we sought to investigate the roles of lncRNA in the kidney injury following intra-arterial contrast exposure by RNA sequencing. Results: We identified 88 differentially expressed known and novel lncRNAs at 12 hours following intra-arterial iodinated contrast medium injection. Functional enrichment analysis implied that these lncRNAs were potentially associated with oxidative stress and DNA damage response. Conclusions:These prefound findings provide the first evidence of lncRNA in the development of CI-AKI.
2021-05-18 | GSE134824 | GEO
Project description:The availability of mesenchymal stem cells in kidney injury repair has been demonstrated. However, the underlying molecular mechanism remains not well understood. Herein, we profiled the altered microRNAs in renal tissiues from cisplatin-induced acute kidney injury (AKI) rats administrated with or without rat bone marrow mesenchymal stem cells, normal kidneys as control. Sprague Dawley rats were administrated with PBS by caudal vein after 24h peritoneal injection of 6mg/mg cisplatin, short for g2. 1×106 MSCs were injected to rats after 24h peritoneal injection of cisplatin, short for g3. Kidneys from healthey rats were used as control, short for g1. Renal tissues were collected at day 5 after treatment. There were 44 micorRNAs changed with significance between g2 and g3, among which 36 microRNAs upregulated and 8 microRNAs downregulated.
2015-03-11 | GSE66761 | GEO
Project description:Renoprotective Effects of Valproic Acid and Dexamethasone in Acute Kidney Ischemia-Reperfusion Injury
| PRJNA252608 | ENA
Project description:We created a rat renal congestion model and investigated the effect of renal congestion on hemodynamics and molecular mechanisms. The inferior vena cava (IVC) between the renal veins was ligated by suture in male Sprague-Dawley rats to increase upstream IVC pressure and induce congestion in the left kidney only. Left kidney congestion reduced renal blood flow, glomerular filtration rate, and increased renal interstitial hydrostatic pressure. Tubulointerstitial and glomerular injury and medullary thick ascending limb hypoxia were observed only in the congestive kidneys. Molecules related to extracellular matrix expansion, tubular injury, and focal adhesion were upregulated in microarray analysis. Renal decapsulation ameliorated the tubulointerstitial injury. Electron microscopy captured pericyte detachment in the congestive kidneys. Transgelin and platelet-derived growth factor receptors, as indicators of pericyte-myofibroblast transition, were upregulated in the pericytes and the adjacent interstitium. With the compression of the peritubular capillaries and tubules, hypoxia and physical stress induce pericyte detachment, which could result in extracellular matrix expansion and tubular injury in renal congestion.
2018-11-14 | GSE114031 | GEO