Single cell RNA sequencing of ischemia reperfused kidneys from Cre- and endothelial cell specific prolylhydroxylase 1, 2, and 3 knockout mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE244064 | GEO | 2023/10/01
REPOSITORIES: GEO
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Project description:We analyzed differences in IRI kidneys between WT and Keap1 KD mice (= Nrf2-activated mice). To identify Nrf2-target genes or metabolic genes in kidneys, we examined the mRNA expression profile both in normal (uninjured) and IRI kidneys (at day1 after unilateral IRI) from mice
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Project description:Current methods to analyze gene expression measure steady-state levels of mRNA. In order to specifically analyze mRNA transcription, a technique has been developed that can be applied in-vivo in intact cells and animals. The technique is referred with the acronym NIAC-NTR (Non Invasive Application and Capture of Newly Transcribed RNA). This method makes use of the cellular pyrimidine salvage pathway and is based on affinity-chromatographic isolation of thiolated mRNA. When combined with data on mRNA steady-state levels, this method is able to assess the relative contributions of mRNA synthesis and degradation/stabilization. It overcomes limitations associated with currently available methods such as mechanistic intervention that disrupts cellular physiology, or the inability to apply the techniques in-vivo. The method was applied to study renal ischemia reperfusion injury, demonstrating its applicability for whole organs in-vivo. Affymetrix GeneChip microarrays were used to detail regulatory mechanisms of mRNA expression and the relative contributions of RNA synthesis and turnover within distinct pathways, and identification of genes expressed at low abundance at the transcriptional level. Experiment Overall Design: The gene expression and regulation program at the RNA level of contralateral mouse kidneys of model IRI-mice was studied. Total RNA, amplified total RNA and specifically enriched newly transcribed RNA was isolated from normal untreated mouse kidneys and from contralateral mouse kidneys of IRI-mice. This experiment allowed detailed regulatory mechanisms in-vivo of mRNA expression and the relative contributions of RNA synthesis and turnover within distinct pathways, and identification of genes expressed at low abundance at the transcriptional level of contralateral kidneys early (3h) after ischemia-reperfusion-injury..
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2009-01-20 | E-GEOD-14373 | biostudies-arrayexpress
Project description:Ischemia/reperfusion injury (IRI) has a major impact on the long-term outcome of renal allografts. However, the mechanisms of IRI related to chronic allograft nephropathy (CAN) are still poorly understood. To address this issue, in a F344 to Lewis transplantation model of the rat, kidneys were either subjected to 20 min. or 24 hours of cold ischemia. A customized cDNA microarray representing 737 immune related genes was used for gene expression analysis after 12 hours and 6 months of engraftment. Thereby showing the 6-month graft function and histology were only moderately deteriorated following short cold ischemic time (20 min.), while prolonged ischemia (24 hrs) accelerated CAN development. Following prolonged cold ischemia already 12 hrs after engraftment about 30 genes were differentially expressed up to >20-fold. This included adhesion molecules, heat shock proteins, transcription factors and chemokines (CXCL10) associated with a strong CD68+ macrophage infiltration. Furthermore we observed a remarkable up-regulation of immunoproteasomes implying a re-organisation of the proteasome complex. This data might explain the higher incidence of alloreactivity following enhanced IRI. After 6 months, the prolonged cold ischemia of 24 hours revealed the significant induction of 4 genes: clusterin, C4, and the CCR7 ligands CCL19/21. This supported the observation of enhanced vasculopathy, humoral alloreactivity and increased tracking of MHC-II+ antigen presenting cells during CAN suggesting them as suitable novel targets for combating IRI. Keywords: transplantation, cold ischemia, inflammation, gene expression profiling Renal allografts from F344 donors were transplanted into unmodified LEW recipients. Before harvesting, grafts were perfused with University of Wisconsin solution at 4°C undergoing 20 min. (group A) or 24 hrs (group B) cold ischemia. Engrafted organs were either removed after 12 hrs (group I-A (n=3) and I-B (n=2)) or after 6 months (group II-A (n=3) and II-B (n=2)). Recipient animals of the group II received CyA treatment for 10 days at a dosage of 1.5 mg/kg. Untreated normal kidneys from F344 rats served as control. RNA from transplanted and untreated (control) rat kidneys were labeled by reverse transcription with Cy5 and Cy3 fluorescence, respectively.
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Project description:Due to organ shortage, the transplantation community are increasingly using kidney from deceased donors such as donation after circulatory death (DCD) and donation after brain death (DBD). However, DCD donation have increased delayed graft function compared to DBD, an underline mechanism is still not well defied at the molecular level. In this study, we employed a rat model to mimic warm ischemia (45 mins) and reperfusion injury (IRI) for 4h and 24h. Apoptotic and tissue histological staining confirmed apoptosis and necrosis occurred at 4h and 24h post IRI respectively. Tissue proteome study revealed acute phase response, coagulation and complement activation and lipid X receptor activation as major pathway altered in intervention kidneys. Metabolomics follow up disclosed an increased level of lipids and fatty acids (FA). Mitochondrial function analysed by mitochondrial complex I activity and oxygen consumption and ATP levels in intervention kidney tissues were maintained 4h post IRI, but was significantly reduced 24h post IRI. Integrated proteo-metabolome analysis discovered an increased FA beta-oxidation 4h post IRI to sustain energy production. Kidney function were declined 24h post IRI indicated by increased blood creatinine and lactate levels. This study provides the frame work for the design of future metabolic intervention strategies to minimize kidney injury.
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