Next generation sequencing of icariin protection against contrast induced acute kidney injury
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA784949 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17074275.fastq.gz | Fastqsanger.gz | |||
| SRR17074276.fastq.gz | Fastqsanger.gz | |||
| SRR17074277.fastq.gz | Fastqsanger.gz | |||
| SRR17074278.fastq.gz | Fastqsanger.gz | |||
| SRR17074279.fastq.gz | Fastqsanger.gz |
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Project description:This study aims to investigate the underlying mechanism of protective effect of icariin in contrast medium induced acute kidney injury.
2024-11-29 | GSE189881 | GEO
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:Renal hypoxia is widespread in acute kidney injury (AKI) of various aetiologies. Hypoxia adaptation, conferred through the hypoxia-inducible factor (HIF), appears to be insufficient. Here we show that HIF activation in renal tubules through Pax8-rtTA-based inducible knockout of von Hippel-Lindau protein (VHL-KO) protects from rhabdomyolysis-induced AKI. In this model, histological observations indicate that injury mainly affects proximal convoluted tubules, with 5% necrosis at d1 and 40% necrosis at d2. HIF-1alpha up-regulation in distal tubules reflects renal hypoxia. However, lack of HIF in proximal tubules suggests insufficient adaptation by HIF. AKI in VHL-KO mice leads to prominent HIF activation in all nephron segments, as well as to reduced serum creatinine, serum urea, tubular necrosis, and apoptosis marker caspase-3 protein. At d1 after rhabdomyolysis, when tubular injury is potentially reversible, HIF mediated protection in AKI is associated with activated glycolysis, cellular glucose uptake and utilization, autophagy, vasodilation, and proton removal as demonstrated by qPCR, pathway enrichment analysis and immunohistochemistry. Together, our data provide evidence for a HIF-orchestrated multi-level shift towards glycolysis as a major mechanism for protection against acute tubular injury. All experiments were carried out in transgenic mice in which selective renal tubular VHL knockout (VHL-KO) was inducible by doxycycline (Reference: Mathia S, Paliege A, Koesters R, Peters H, Neumayer HH, Bachmann S, Rosenberger C. Action of hypoxia-inducible factor in liver and kidney from mice with Pax8-rtTA-based deletion of von Hippel-Lindau protein. Acta Physiol (Oxf). 2013; 207(3):565-76.). Four groups of animals were used: 1) controls: untreated mice; 2) VHL-KO: injected with doxycycline (0.1 mg per 10 g body weight SC), 4 days prior to sacrifice; 3) AKI: rhabdomyolysis; 4) VHL-KO/AKI: doxycycline plus rhabdomyolysis. To induce AKI, 50% glycerol (0.05 ml per 10 g body weight) was injected IM into the left hind limb under isoflurane narcosis. Drinking water was withdrawn between 20 h prior and 24 h after glycerol injection.
2013-09-05 | E-GEOD-44925 | biostudies-arrayexpress
Project description:Renal hypoxia is widespread in acute kidney injury (AKI) of various aetiologies. Hypoxia adaptation, conferred through the hypoxia-inducible factor (HIF), appears to be insufficient. Here we show that HIF activation in renal tubules through Pax8-rtTA-based inducible knockout of von Hippel-Lindau protein (VHL-KO) protects from rhabdomyolysis-induced AKI. In this model, histological observations indicate that injury mainly affects proximal convoluted tubules, with 5% necrosis at d1 and 40% necrosis at d2. HIF-1alpha up-regulation in distal tubules reflects renal hypoxia. However, lack of HIF in proximal tubules suggests insufficient adaptation by HIF. AKI in VHL-KO mice leads to prominent HIF activation in all nephron segments, as well as to reduced serum creatinine, serum urea, tubular necrosis, and apoptosis marker caspase-3 protein. At d1 after rhabdomyolysis, when tubular injury is potentially reversible, HIF mediated protection in AKI is associated with activated glycolysis, cellular glucose uptake and utilization, autophagy, vasodilation, and proton removal as demonstrated by qPCR, pathway enrichment analysis and immunohistochemistry. Together, our data provide evidence for a HIF-orchestrated multi-level shift towards glycolysis as a major mechanism for protection against acute tubular injury.
2013-09-05 | GSE44925 | GEO
Project description:Contrast-induced acute kidney injury (CI-AKI) is a serious complication of percutaneous coronary intervention (PCI). Emerging evidence suggests that messengerRNAs (mRNAs) and long non-coding RNAs (lncRNAs) could serve as biomarkers for various diseases.
2023-11-17 | GSE248078 | GEO
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:Novel biomarkers for contrast-induced acute kidney injury identified from RNA sequencing data
| PRJNA1041736 | ENA
Project description:Purpose: The pathogenesis of contrast-induced acute kidney injury (CI-AKI) has not yet been clearly understood. miRNAs are important mediators which normally work by post-transcriptional degradation of target mRNAs. Emerging evidence indicated a number of differentially expressed miRNAs in CI-AKI following intravenous contrast medium injection. However, there exist differences in the pathological mechanisms and incidences of CI-AKI between intravenous and intra-arterial contrast administration. We aimed to investigate the critical roles of dysregulated miRNAs and the correlated mRNAs in the kidney injury following intra-arterial contrast exposure. Methods: Based on a reliable CI-AKI rat model, we sought to investigate the roles of miRNA-mRNA interactions in the kidney injury following intra-arterial contrast exposure using the Illumina Genome Analyzer IIx. Results: In the study, 36 differentially expressed mature miRNAs were identified ( fold change > 1.5 and p value < 0.05) in the kidney of CI-AKI rats (n = 3) compared with controls (n = 3), consisting of 23 up-regulated and 13 down-regulated ones. Bioinformatics analysis revealed that Wnt, TGF-β, and AMPK signaling pathways were most likely to be modulated by these dysregulated miRNAs. Around 453 dysregulated genes ( fold change > 2.0 and p value < 0.05) were identified. Integrated analysis revealed 2037 putative miRNA-mRNA pairs with negative correlations. Of which, 6 differential miRNAs and 13 genes were selected for further quantitative real-time polymerase chain reaction validation (n = 6 for each group), and a well correspondence between the 2 techniques was observed. Conclusions: In conclusion, our present study contributes to the first evidence of miRNA-mRNA regulations in the development of kidney injury following an intra-arterial contrast injection route. These novel findings provide insights into the underlying mechanisms of CI-AKI.
2020-04-10 | GSE130796 | GEO
Project description:Purpose:The pathogenesis of contrast-induced acute kidney injury (CI-AKI) has not yet been clearly understood. miRNAs are important mediators which normally work by post-transcriptional degradation of target mRNAs. Emerging evidence indicated a number of differentially expressed miRNAs in CI-AKI following intravenous contrast medium injection. However, there exist differences in the pathological mechanisms and incidences of CI-AKI between intravenous and intra-arterial contrast administration. We aimed to investigate the critical roles of dysregulated miRNAs and the correlated mRNAs in the kidney injury following intra-arterial contrast exposure. Methods:Based on a reliable CI-AKI rat model, we sought to investigate the roles of miRNA-mRNA interactions in the kidney injury following intra-arterial contrast exposure using the Illumina Genome Analyzer IIx. Results:In the study, 36 differentially expressed mature miRNAs were identified ( fold change > 1.5 and p value < 0.05) in the kidney of CI-AKI rats (n = 3) compared with controls (n = 3), consisting of 23 up-regulated and 13 down-regulated ones. Bioinformatics analysis revealed that Wnt, TGF-β, and AMPK signaling pathways were most likely to be modulated by these dysregulated miRNAs. Around 453 dysregulated genes ( fold change > 2.0 and p value < 0.05) were identified. Integrated analysis revealed 2037 putative miRNA-mRNA pairs with negative correlations. Of which, 6 differential miRNAs and 13 genes were selected for further quantitative real-time polymerase chain reaction validation (n = 6 for each group), and a well correspondence between the 2 techniques was observed. Conclusions:In conclusion, our present study contributes to the first evidence of miRNA-mRNA regulations in the development of kidney injury following an intra-arterial contrast injection route. These novel findings provide insights into the underlying mechanisms of CI-AKI.
2020-04-10 | GSE130795 | GEO