Genome-wide analysis of long noncoding RNAs and mRNAs associated with contrast-induced acute kidney injury
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PROVIDER: PRJNA556583 | ENA |
REPOSITORIES: ENA
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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: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: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:Long noncoding RNA profile in the mouse plasma after ischemia-reperfusion injury (IRI). In the study presented here, we mixed the plasma from three mouse after IRI and identified the genome-wide expression level of lncRNAs.
2015-12-31 | E-GEOD-60726 | biostudies-arrayexpress
Project description:Long noncoding RNA profile in the mouse plasma after ischemia-reperfusion injury (IRI).
2015-12-31 | GSE60726 | 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
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:This experiment compared the expression of mRNAs and noncoding RNAs during myoblast differentiation. The primary aim of the experiment was to identify ncRNAs that were differentially expressed during myotube formation.
2008-12-01 | E-TABM-575 | biostudies-arrayexpress
Project description:Long noncoding RNA profile in the mouse left kidney and right kidney.
2016-12-01 | GSE60723 | GEO