The transcriptional response to unilateral nephrectomy with and without ischemia-reperfusion injury
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE100540 | GEO | 2017/11/04
SECONDARY ACCESSION(S): PRJNA392078
REPOSITORIES: GEO
Similar Datasets
Project description:Purpose: Experiments were done in mice undergoing unilateral nephrectomy (UNx) and sham nephrectomy. At specific time points (24 hours and 72 hours) after surgery, the earliest first portion of the kidney proximal tubule (PT-S1) and the cortical collecting duct (CCD) were manually micro-dissected and utilized for transcriptomic analysis by single-tubule small sample RNA-Seq and single-tubule ATAC seq. Methods: We carried out ATAC-sequencing in microdissected ealiest portion of proximal tubules (PT-S1) from mice with or without (sham) unilateral nephrectomy (UNx). Each group (Sham or UNx) has 3 biological replicates. Results and conclusion: ATAC-seq peaks in microdissected PT-S1 revealed a predominance of binding site motifs corresponding to PPARα.
2022-08-14 | GSE211022 | GEO
Project description:Purpose: Experiments were done in mice undergoing unilateral nephrectomy (UNx) and sham nephrectomy. At specific time points (24 hours and 72 hours) after surgery, the earliest first portion of the kidney proximal tubule (PT-S1) and the cortical collecting duct (CCD) were manually micro-dissected and utilized for transcriptomic analysis by single-tubule small sample RNA-Seq. Methods: We carried out RNA-sequencing in microdissected ealiest portion of proximal tubules (PT-S1) or cortical collecting duct (CCD) from mice with or without (sham) unilateral nephrectomy (UNx). Each group (Sham or UNx) has 3-5 biological replicates. Results and conclusion: RNA-Seq in microdissected PT-S1 at 24 hours showed that peroxisome proliferator-activated receptor alpha (PPARα) target genes were strongly upregulated. RNA-Seq in microdissected PT-S1 at 72 hours showed that cell cycle related genes were strongly upregulated. RNA-Seq in microdissected CCD at both 24 hours and 72 hours showed that cell cycle related genes were strongly upregulated.
2022-08-14 | GSE211021 | GEO
Project description:To examine genome wide transcriptional changes in the heart of 5/6 nephrectomy CKD mice, we performed microarray analysis using the Affymetrix Clariom S array.
2020-01-04 | GSE143031 | GEO
Project description:Comparing the effect of unilateral ischemia-reperfusion injury (IRI) or sham operation (sIRI) with delayed contralateral nephrectomy (Nx) or sham operation (sNx) in mouse kidney. IRI was performed on day 0 and the contralateral kidney was removed on day 7. Mice were sacrificed on day 8. Four animals were selected from the sham IRI-sham Nx and sham IRI-Nx groups and six animals were selected from the IRI-sham Nx and IRI-Nx groups for miRNA microArray analysis on the base of their proinflammatory (TNF-α and IL-6 and CCL2) and immune system-related (Complement component 3) mRNA expression levels.
2020-09-01 | GSE157221 | GEO
Project description:We had analysed gene expression profile of brain in SCI rat by MSC. Compared with MSC intravenous and vehicle injection at SCI day3. We used Clariom D / Gene Chip® Rat Transcriptome Array (RTA 1.0., Affymetrix, Santa Clara, CA, USA).
2018-09-01 | GSE108168 | GEO
Project description:Experiments in rodents have shown that kidney ischemia/reperfusion injury (IRI) facilitates lung injury and inflammation. To identify potential ischemia-specific lung molecular pathways involved, we conducted global gene expression profiling of lung 6 or 36 hours following 1) bilateral kidney IRI, 2) bilateral nephrectomy (BNx), and 3) sham laparotomy in C57BL/6J mice. Total RNA from whole lung was isolated and hybridized to 430MOEA (22,626 genes) GeneChips (n=3/group). Keywords: different time points after different treatments
2007-05-30 | GSE6730 | GEO
Project description:Compensation is a physiological response that occurs during chemical exposure to maintain homeostasis. Because compensatory responses are not usually considered adverse effects, it is important to understand compensatory mechanisms for chemical risk assessment. Although the kidney is a major target organ for toxicity, there is controversy over whether hyperplasia or hypertrophy contributes to the compensatory mechanism, and there is limited information to apply for chemical risk assessment. In the current study, compensatory mechanisms of the kidney were investigated in a unilateral nephrectomy (UNx) model using adult male and female rats. In residual kidneys of male and female rats after UNx, 5-bromo-2'-deoxyuridine-labeling indices and mRNA expression of cell cycle-related genes were increased, although there were no fluctuations in mRNA expression of transforming growth factor-β1, which contributes to hypertrophy in renal tubules. Pathway analysis using mRNA expression data from a cDNA microarray revealed that canonical pathways related to cell proliferation were mainly activated and that forkhead box M1 (FOXM1) was an upstream regulator of compensatory cell proliferation in residual kidneys of male and female rats. cDNA microarray for microRNAs (miRNAs) demonstrated that 9 miRNAs were downregulated in residual kidneys, and mRNA/miRNA integrated analysis indicated that miRNAs were associated with the expression of factors downstream of FOXM1. Overall, these results suggested that FOXM1-mediated hyperplasia rather than hypertrophy contributed to compensatory mechanisms in the kidney and that miRNAs regulated downstream FOXM1 signaling. These results will be beneficial for evaluating nephrotoxicity in chemical risk assessment and for developing new biomarkers to predict nephrotoxicity.
2020-04-01 | GSE144263 | GEO
Project description:Compensation is a physiological response that occurs during chemical exposure to maintain homeostasis. Because compensatory responses are not usually considered adverse effects, it is important to understand compensatory mechanisms for chemical risk assessment. Although the kidney is a major target organ for toxicity, there is controversy over whether hyperplasia or hypertrophy contributes to the compensatory mechanism, and there is limited information to apply for chemical risk assessment. In the current study, compensatory mechanisms of the kidney were investigated in a unilateral nephrectomy (UNx) model using adult male and female rats. In residual kidneys of male and female rats after UNx, 5-bromo-2'-deoxyuridine-labeling indices and mRNA expression of cell cycle-related genes were increased, although there were no fluctuations in mRNA expression of transforming growth factor-β1, which contributes to hypertrophy in renal tubules. Pathway analysis using mRNA expression data from a cDNA microarray revealed that canonical pathways related to cell proliferation were mainly activated and that forkhead box M1 (FOXM1) was an upstream regulator of compensatory cell proliferation in residual kidneys of male and female rats. cDNA microarray for microRNAs (miRNAs) demonstrated that 9 miRNAs were downregulated in residual kidneys, and mRNA/miRNA integrated analysis indicated that miRNAs were associated with the expression of factors downstream of FOXM1. Overall, these results suggested that FOXM1-mediated hyperplasia rather than hypertrophy contributed to compensatory mechanisms in the kidney and that miRNAs regulated downstream FOXM1 signaling. These results will be beneficial for evaluating nephrotoxicity in chemical risk assessment and for developing new biomarkers to predict nephrotoxicity.
2020-04-01 | GSE144262 | GEO
Project description:Compensation is a physiological response that occurs during chemical exposure to maintain homeostasis. Because compensatory responses are not usually considered adverse effects, it is important to understand compensatory mechanisms for chemical risk assessment. Although the kidney is a major target organ for toxicity, there is controversy over whether hyperplasia or hypertrophy contributes to the compensatory mechanism, and there is limited information to apply for chemical risk assessment. In the current study, compensatory mechanisms of the kidney were investigated in a unilateral nephrectomy (UNx) model using adult male and female rats. In residual kidneys of male and female rats after UNx, 5-bromo-2'-deoxyuridine-labeling indices and mRNA expression of cell cycle-related genes were increased, although there were no fluctuations in mRNA expression of transforming growth factor-β1, which contributes to hypertrophy in renal tubules. Pathway analysis using mRNA expression data from a cDNA microarray revealed that canonical pathways related to cell proliferation were mainly activated and that forkhead box M1 (FOXM1) was an upstream regulator of compensatory cell proliferation in residual kidneys of male and female rats. cDNA microarray for microRNAs (miRNAs) demonstrated that 9 miRNAs were downregulated in residual kidneys, and mRNA/miRNA integrated analysis indicated that miRNAs were associated with the expression of factors downstream of FOXM1. Overall, these results suggested that FOXM1-mediated hyperplasia rather than hypertrophy contributed to compensatory mechanisms in the kidney and that miRNAs regulated downstream FOXM1 signaling. These results will be beneficial for evaluating nephrotoxicity in chemical risk assessment and for developing new biomarkers to predict nephrotoxicity.
2020-04-01 | GSE144261 | GEO
Project description:Experiments in rodents have shown that kidney ischemia/reperfusion injury (IRI) facilitates lung injury and inflammation. To identify potential ischemia-specific lung molecular pathways involved, we conducted global gene expression profiling of lung 6 or 36 hours following 1) bilateral kidney IRI, 2) bilateral nephrectomy (BNx), and 3) sham laparotomy in C57BL/6J mice. Total RNA from whole lung was isolated and hybridized to 430MOEA (22,626 genes) GeneChips (n=3/group). Experiment Overall Design: All procedures were approved by the Johns Hopkins Animal Care and Use Committee, and were consistent with the National Institutes of Health (NIH) Guide for the Care and Use of Laboratory Animals. Male 6-8 week-old mice (C57BL6/J), weighing approximately 25-30 grams were obtained from Jackson Laboratory (Bar Harbor, ME) and housed under pathogen-free conditions according to NIH guidelines at least five days prior to operative procedures. Experiment Overall Design: Animals were placed on a heating blanket and underwent midline laparotomy with isolation of bilateral renal pedicles. For mice assigned to experimental ischemia-reperfusion injury (IRI), a non-traumatic microvascular clamp was applied across both renal pedicles for 60 minutes. After the allotted ischemia time, the clamps were gently removed, the animals administered 1 ml of sterile saline intraperitoneally, and the incision closed in two layers with 4-0 silk suture. The animals were then allowed to recover with free access to food and water. Sham animals underwent the identical procedure without placement of the vascular clamps. The mice assigned to bilateral nephrectomy (BNx) underwent similar procedures except both renal pedicles were ligated with 5-0 silk suture and the kidneys removed. At 6 or 36 hours following the experimental procedure, the mice were euthanized by exsanguination under pentobarbital anesthesia and lung tissues collected for analysis.
2008-06-15 | E-GEOD-6730 | biostudies-arrayexpress