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Transcriptional analysis of kidney infiltrating T cells after ischemia reperfusion injury reveals a pathophysiologic role for the chemokine (C-C motif) receptor 5

ABSTRACT: We examined the transcriptional responses in kidney infiltrating T cells 6 hrs after IRI

ORGANISM(S): Mus musculus

PROVIDER: GSE23747 | GEO | 2011/08/31

SECONDARY ACCESSION(S): PRJNA130761

REPOSITORIES: GEO

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Transcriptional analysis of kidney infiltrating T cells after ischemia reperfusion injury reveals a pathophysiologic role for the chemokine (C-C motif) receptor 5

Project description:We examined the transcriptional responses in kidney infiltrating T cells 6 hrs after IRI CD3 (+) T cells were purified applying magnetic beads to mononuclear cells extracted from kidney by percoll gradient methods. The total T-cell RNA was isolated, and trabscript abundance measured with array-based PCR

2011-08-31 | E-GEOD-23747 | biostudies-arrayexpress

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Murine Kidney cells: Control versus Ischemia reperfusion injury

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2011-07-31 | E-GEOD-29495 | biostudies-arrayexpress

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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.

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Transcriptomics of Human Liver Ischemia and Reperfusion Injury

Project description:For orthotopic liver transplants, ischemia-reperfusion injury (IRI) is known to compromise allograft survival. To better understand the transcriptomics of immune responses underlying liver transplant IRI, RNA-seq was performed on liver biopsies from 23 IRI+ and 17 IRI- patients, both pre-transplant and post-transplant. Genes that are differentially expressed in IRI+ samples, along with the pathways enriched for by those genes, were identified.

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Glutamine attenuates renal ischemia-reperfusion injury and prevents acute kidney damage

Project description:Acute kidney injury (AKI) represents a common complication in critically ill patients that is associated with an increased morbidity and mortality. Currently, no effective treatment options are available. Here, we show that glutamine significantly attenuates leukocyte recruitment and inflammatory signaling in human and murine tubular epithelial cells (TECs). In a murine AKI model induced by ischemia-reperfusion-injury (IRI) we show that glutamine causes transcriptomic and proteomic reprogramming in renal TECs and neutrophils, resulting in decreased epithelial apoptosis, neutrophil recruitment and improved mitochondrial functionality and respiration provoked by an ameliorated oxidative phosphorylation. We identify the proteins glutamine gamma glutamyltransferase 2 (Tgm2) and apoptosis signal-regulating kinase (Ask1) as the major targets of glutamine in apoptotic signaling. Increased Tgm2 expression and reduced Ask1 activation result in decreased JNK activation leading to a diminished mitochondrial intrinsic apoptosis in kidneys upon IRI-induced AKI and under hypoxia or following TNFα-treatment of TECs. Consequently, glutamine administration attenuated kidney injury in vivo during AKI progression as well as TEC viability in vitro under inflammatory and hypoxic conditions.

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Calycosin inhibited MIF-mediated inflammatory chemotaxis of macrophages to ameliorate ischemia reperfusion-induced acute kidney injury

Project description:Acute kidney disease caused by ischemia-reperfusion (IRI-AKI) is characterized by ectopic inflammation and tubular injury, in which macrophage infiltration and inflammatory activation play a critical pathogenic role. Calycosin is an active flavone from the root of Astragalus membranaceus and shows anti-inflammatory effects in various diseases. In this study, we investigated the renoprotective role of calycosin against IRI-AKI and the underlying mechanism. Our results showed that calycosin treatment reduced the levels of serum creatinine and urea nitrogen along with attenuated tubular necrosis and cast formation in IRI-AKI mice. Calycosin significantly suppressed the activation of NF-κB signaling and the expression of inflammatory mediators IL-1β and TNF-α in IRI-AKI kidneys. In vitro, calycosin inhibited LPS-induced inflammatory activation in RAW 264.7 cells. Interestingly, RNA-seq revealed that calycosin remarkably down-regulated chemotaxis-related pathways in RAW 264.7 cells. Among the differentially expressed genes, Ccl2/MCP-1, a critical chemokine mediating macrophage inflammatory chemotaxis, was down-regulated in both LPS-stimulated RAW 264.7 cells and IRI-AKI kidneys. Consistently, calycosin treatment attenuated macrophage infiltration in the IRI-AKI kidneys. Importantly, in combination with target prediction, molecular docking, and surface plasmon resonance, we showed that calycosin can directly bind to macrophage migration inhibitory factor (MIF). Functionally, calycosin abrogated MIF-stimulated NF-κB signaling activation and Ccl2 expression and MIF-mediated chemotaxis in RAW 264.7 cells without influencing its expression. Collectively, calycosin protects from IRI-AKI by suppressing MIF-mediated macrophage inflammatory chemotaxis. Calycosin could be a promising candidate medicine for clinical treatment of IRI-AKI.

2024-07-28 | GSE247263 | GEO

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Project description:To better understand the pathogenesis of AKI-to-CKD transition and specifically the mechanism of kidney atrophy, we compared the kidney response to an identical time of ischemic injury between mice subjected to unilateral ischemia/reperfusion (U-IRI) to induce atrophy and those subjected to unilateral IRI with contralateral nephrectomy (IRI/CL-NX) to induce adaptive repair. We performed single cell RNA-sequencing (scRNA-seq) analyses on day 14 after injury to identify major cell types in the kidney and the differential transcriptional response between the models in each cell type.

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