MicroRNAs profiles of contrast-induced acute kidney injury rats
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE81400 | GEO | 2016/05/14
SECONDARY ACCESSION(S): PRJNA321466
REPOSITORIES: GEO
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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 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:MicroRNAs (miRNAs) are endogenous small RNAs of 18–23 nucleotides that regulate gene expression. Recently, plasma miRNAs have been investigated as biomarkers for various diseases. In the present study, we assessed whether the miRNA expression profiles of tubular tissues could discriminate proximal tubule injury and diagnose acute kidney injury (AKI) and the renal tubular dysfunction without morphological changes.
2015-03-17 | GSE66195 | GEO
Project description:MicroRNAs (miRNAs) are endogenous small RNAs of 18–23 nucleotides that regulate gene expression. Recently, plasma miRNAs have been investigated as biomarkers for various diseases. In the present study, we assessed whether the miRNA expression profiles of tubular tissues could discriminate proximal tubule injury and diagnose acute kidney injury (AKI) and the renal tubular dysfunction without morphological changes.
2015-03-17 | GSE66134 | 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: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: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:Microarray analysis of human kidneys with acute kidney injury (AKI) has been limited because such kidneys are seldom biopsied. However, all kidney transplants experience AKI, and early kidney transplants without rejection are an excellent model for human AKI: they are screened to exclude chronic kidney disease, frequently biopsied, and have extensive follow-up. We used histopathology and microarrays to compare indication biopsies from 28 transplants with AKI to 11 pristine protocol biopsies of stable transplants. Kidneys with AKI showed increased expression of 394 injury-repair response associated transcripts, including many known epithelial injury molecules (e.g. ITGB6, LCN2), tissue remodeling molecules (e.g. VCAN), and inflammation molecules (S100A8, ITGB3). Many other genes also predict the phenotype, depending on statistical filtering rules, including AKI biomarkers as HAVCR1 and IL18. Most mouse orthologs of the top injury-repair transcripts were increased in published mouse AKI models. Pathway analysis of the injury-repair transcripts revealed similarities to cancer, development, and cell movement. The injury-repair transcript score AKI kidneys correlated with reduced function, future recovery, brain death, and need for dialysis, but not future graft loss. In contrast, histologic features of "acute tubular injury" did not correlate with function or with the molecular changes. Thus the injury-repair associated transcripts represent a massive coordinate injury-repair response of kidney parenchyma to AKI, similar to mouse AKI models, and provide an objective measure for assessing the severity of AKI in kidney biopsies and validation for the use of many AKI biomarkers. AKI biopsies sample names and CEL files are from GSE21374. All consenting renal transplant patients undergoing biopsies for cause as standard of care between 09/2004 and 10/2007 at the university of Alberta or between 11/2006 and 02/2007 at the University of Illinois were included in the analysis. In addition to the cores required for standard histopathology, we collected one core for gene expression studies. the relationship between gene expression in the biopsy and subsequent graft loss was analyzed. This dataset is part of the TransQST collection.
2012-02-21 | E-GEOD-30718 | biostudies-arrayexpress
Project description:Two metrics, a rise in serum creatinine concentration and a decrease in urine output, are considered tantamount to the injury of the kidney tubule and the epithelial cells thereof (AKI).Yet neither criterion emphasizes the etiology or the pathogenetic heterogeneity of acute decreases in kidney excretory function. In fact, whether decreased excretory function due to contraction of the extracellular fluid volume (vAKI) or due to intrinsic kidney injury (iAKI) actually share pathogenesis and should be aggregated in the same diagnostic group remains an open question. To examine this possibility, we created mouse models of iAKI and vAKI that induced a similar increase in serum creatinine concentration. Using laser microdissection to isolate specific domains of the kidney, followed by RNA sequencing, we found that thousands of genes responded specifically to iAKI or to vAKI, but very few responded to both stimuli. In fact, the activated gene sets comprised different, functionally unrelated signal transduction pathways and were expressed in different regions of the kidney. Moreover, we identified distinctive gene expression patterns in human urine as potential biomarkers of either iAKI or vAKI, but not both. Hence, iAKI and vAKI are biologically unrelated, suggesting that molecular analysis should clarify our current definitions of acute changes in kidney excretory function.
2016-12-01 | GSE81741 | GEO
Project description:In deceased donor kidney transplantation, acute kidney injury (AKI) prioir to surgery is a major determinant of delayed graft function (DGF), but AKI is histologically silent and difficult to assess. We hypothesized that a molecular measurement of AKI would add power to conventional risk assessments to predict the early poor allograft function at first week post transplantation. We performed microarrays on implantation biopsies taken during reperfusion in 70 deceased donor kidneys from 53 donors. Early poor function was classified by two definitions on day 7 post-transplantation: serum creatinine greater than 265 umol/L (3 mg/dL) or the requirement for dialysis. Donor age and related risk scores (Irish, Schold, KDRI) associated with worse early function, as expected, but histologic features (glomerulosclerosis; pathology risk scores (Remuzzi, MAPI)) correlated with donor age but not with poor function. However, molecular AKI signal, previously defined in kidneys with early injury, was the best single predictor of poor allograft function. The combination of donor age and the AKI signal improved the prediction of poor function. In addition, asssessments of tissue quality particularly donor age, Banff ct, Irish and KDRI scores, showed negative correlative trend with late graft function, whereas the AKI signal did not. Thus donor age and the molecular AKI signal are the main predictors of early impaired function, but have little impact on survival.
2013-02-13 | E-GEOD-37838 | biostudies-arrayexpress