Mus musculus
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PROVIDER: PRJNA291701 | ENA |
REPOSITORIES: ENA
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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 We performed microarray analyses using 1) Injured kidneys at day 1 after unilateral IRI, and 2) intact kidneys from mice which did not undergo UIRI. Samples were harvested from Keap1 KD mice and WT mice, n = 2 each,
2016-04-01 | E-GEOD-71647 | biostudies-arrayexpress
Project description:Ischemia-reperfusion injury (IRI) is a well-known model for acute kidney injury (AKI).
We applied proteomic analysis to detect membrane proteins from IRI mouse kidneys. The analysis set are composed of negative control (sham operation), samples of 4-hour after IRI, and samples of 8-hour IRI.
2021-09-30 | PXD020708 | JPOST Repository
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
2016-04-01 | GSE71647 | GEO
Project description:Preconditioning strategies like caloric restriction (CR) and hypoxic preconditioning (HP) show remarkable protective effects in animal models of acute kidney injury (AKI). Since the underlying molecular effects are still not fully understood we performed an experiment directly comparing CR and HP in a murine model of ischemia-reperfusion injury (IRI) of the kidney. 8 to 12-week-old, male C57BL6/J mice were either put to 4 weeks of caloric restriction (70% of normal food intake) or placed in a hypoxic chamber (8%O2) for 3 consecutive days prior to IRI. Whole kidneys were used for transcriptional analysis (RNAseq) before and after ischemia-reperfusion injury to look for common effects of both modes of preconditioning.
2019-12-31 | E-MTAB-7982 | biostudies-arrayexpress
Project description:Purpose: The different ischemic time of Ischemia-reperfusion-injury (IRI) mouse models resulted in different outcomes, severe IRI led to chronic kidney disease, while mild IRI led to the recovery of kidneys. We isolated tubules from mice from each group. The goals of this study are to compare differentially expressed mRNAs, lncRNAs and circRNAs among severe IRI-injured tubules, mild IRI-injuried tubules and control mouse tubules.
2022-04-20 | GSE179506 | GEO
Project description:Ischemia reperfusion injury (IRI) in organ transplantation remains a significant problem with limited alternative therapeutic options. Organs that undergo significant damage during IRI, particularly those enduring long warm ischemia times, undergo significant delayed graft function (DGF) after reperfusion and tend to have greater complications long term with the onset of chronic rejection. The gas molecule carbon monoxide (CO) has emerged as an agent that can suppress IRI in rodent models of solid organ transplantation. Since the use of CO is a potential therapeutic modality in humans, we tested if CO can prevent DGF in a pig model of kidney transplantation Keywords: stress response, treatment response 18 Samples from pig kidneys, two naïve controls, two timepoints, two conditions, 4 replicates
2009-01-20 | E-GEOD-14373 | biostudies-arrayexpress
Project description:Fibroblasts are present in every organ. While the role fibroblasts in chronic diseases such as fibrosis or tumor expression has been extensively explored, little is known about their physiological role. The kidney possesses a unique capacity to recover from even severe acute injury. We study molecular mechanisms of this intrinsic repair capacity in the mouse model of ischemia-reperfusion (IR). In this model, the renal artery and vein are clamped for 45 min, leading to acute kidney injury. The kidney spontaneously recovers from such IR injury within 14 days. IR kidney injury is associated with a transient accumulation of fibroblasts in the diseased tissue. We hypothesized that fibroblasts aid the repair of acute IR injury in the kidney. To elucidate how FSP1+ fibroblasts may contribute to the repair of kidney injury, we undertook a global unbiased approach to compare gene expression profiles of fibroblasts isolated from kidneys post-IRI and from control kidneys by FACS sorting. To investigate the role fibroblasts may play in the repair of kidney inhury, we performed ischemia reperfusion injury surgery on transgenic mice in which the FSP-1 promoter drives EGFP expression. Kidney injury peaks at day 3 post-IRI, followed by spontaneous regeration that restores nearly perfect kidney architecture and health by day 10. Fibroblasts are thought to possibly play a role in this process, as they are normally rare in the healthy kidney, acute kidney injury is associated with a transient accumulation of interstitial fibroblasts, but whether they may help repair the acute kidney injury or in fact could contribute to the damage is not known. To compare the gene expression profiles of normal fibroblasts and those from post-ischemic kidneys, we sacrificed control FSP1-GFP mice and the FSP1-GFP mice three days post-IRI. We generated single-cell suspensions from both the post-IRI and control kidneys, and then isolated FSP1-GFP+ cells by FACS sorting that, when cultured on plastic, displayed typical fibroblast morphology. Total RNA was immediately extracted from the sorted cells and amplified to produce enough for a array. We biotinylated five of the samples from post-ischemic kidneys and three of the control (non-ischemic) kidneys and used Affymetrix 3' Arrays to examine differences in gene expression profiles between the two groups that may she some light on what role, if any, fibroblasts play in the spontaneous healing of the kidney after acute kidney injury. We performed ischemia reperfusion surgery in FSP1-GFP mice, and at day 3, we sacrificed the mice, isolated FSP1-GFP positive cells from both IR and normal control kidneys by FACS sorting, extracted total RNA from the isolated FSP1-GFP cells and used Affymetrix Mouse Expression Array 430 2.0 microarrays to perform gene expression profiling of the samples. All told, we performed the FACS Sorting, RNA extration, and hybridization with 5 ischemic kidneys and 3 normal kidneys. Fibroblasts, acute kidney injury, repair, comparative gene expression profiling, microarrays, FACS sorting, role in healing
2014-10-28 | E-GEOD-62732 | biostudies-arrayexpress
Project description:Ischemia/reperfusion injury (IRI) is a hallmark of tissue injury in donation after circulatory death (DCD) kidneys. The implementation of hypothermic machine perfusion (HMP) provides a platform for repair of DCD kidneys. Doxycycline administration has shown protective effects during IRI. Here, we explore the impact of doxycycline on proteolytic degradation mechanisms and the urinary proteome of perfused kidney grafts. Porcine kidneys underwent 30 min of warm ischemia, 24 h of oxygenated HMP (control/doxycycline) and 240 min of ex-vivo reperfusion. A high-efficiency undecanal-based N-termini enrichment workflow (HUNTER) was performed to identify the tissue degradome. In addition, a proteomic analysis was applied on urine samples collected during reperfusion using label-free quantitation (LFQ) mass spectrometry. Hierarchical clustering showed distinctive clustering profiles between urine samples collected at T15 min (metabolism) and T240 min (complement and coagulation). At T10, significantly more degraded proteins were observed in perfusates of the control group. At T240, significantly more degraded proteins were observed in the doxycycline group, indicating that doxycycline alters protein degradation during HMP. In conclusion, doxycycline administration during HMP led to significant proteomic differences including protective effects by attenuating urinary NGAL levels. Ultimately, we unravelled multiple pathways that undergo alterations during machine perfusion that can be targeted to attenuate IRI induced injury.
2022-08-12 | PXD029599 | Pride
Project description:Hepatic ischemia-reperfusion injury (IRI) is a common complication occurs during hepatic resection and transplantation. However, the mechanisms underlying hepatic IRI have not been fully elucidated. Here, we aim to explore the role of fibroblast growth factor 18 (FGF18) in hepatic IRI. In this work, we find that Hepatic stellate cells (HSCs) secrete FGF18 and alleviates hepatocytes injury. HSCs-specific FGF18 deletion largely aggravates hepatic IRI. Mechanistically, FGF18 treatment reduces the levels of ubiquitin carboxyl-terminal hydrolase 16 (USP16), leading to increased ubiquitination levels of Kelch Like ECH Associated Protein 1 (KEAP1) and the activation of nuclear factor erythroid 2-related factor 2 (Nrf2). Furthermore, USP16 interacts and deubiquitinates KEAP1. More importantly, Nrf2 directly binds to the promoter of USP16 and forms a negative feedback loop with USP16. Collectively, our results show FGF18 alleviates hepatic IRI by USP16/KEAP1/Nrf2 signaling pathway in male mice, suggesting that FGF18 represents a promising therapeutic approach for hepatic IRI.
2023-09-05 | GSE242032 | GEO
Project description:Time course experiments involving bilateral renal ischemia reperfusion injury (IRI) in C57BL/6J mice (0 hr control, 20 min bilateral ischemia without reperfusion, 4, 16, 24, 36, 48, and 72 hrs post IRI). This dataset also includes IRI at 48 hrs and 72 hrs in Azin1 A-to-I locked and Azin1 A-to-I uneditable mice.
2024-09-30 | GSE267650 | GEO