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Immune-mediated Tubule Atrophy Promotes Acute Kidney Injury to Chronic Kidney Disease Transition

ABSTRACT: Immune-mediated Tubule Atrophy Promotes Acute Kidney Injury to Chronic Kidney Disease Transition

PROVIDER: PRJNA811238 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18175853.fastq.gz	Fastqsanger.gz
	SRR18175854.fastq.gz	Fastqsanger.gz
	SRR18175855.fastq.gz	Fastqsanger.gz
	SRR18175856.fastq.gz	Fastqsanger.gz
	SRR18175857.fastq.gz	Fastqsanger.gz

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Immune-mediated Tubule Atrophy Promotes Acute Kidney Injury to Chronic Kidney Disease Transition

Project description:Incomplete repair after acute kidney injury (AKI) is associated with progressive loss of tubular cell function and development of chronic kidney disease (CKD). Here, we compared the kidney single-cell transcriptomes from the mice subjected to either unilateral ischemia-reperfusion kidney injury with contralateral nephrectomy (IRI/CL-NX, in which tubule repair predominates) or unilateral IRI with contralateral kidney intact (U-IRI, in which fibrosis and atrophy predominates) to investigate the mechanism(s) underlying transition to CKD following AKI.

2022-06-30 | GSE197626 | GEO

Immune-mediated tubule atrophy promotes acute kidney injury to chronic kidney disease transition

Project description:Incomplete repair after acute kidney injury can lead to development of chronic kidney disease. To define the mechanism of this response, we compared mice subjected to identical unilateral ischemia-reperfusion kidney injury with either contralateral nephrectomy (where tubule repair predominates) or contralateral kidney intact (where tubule atrophy predominates). By day 14, the kidneys undergoing atrophy had more macrophages with higher expression of chemokines, correlating with a second wave of proinflammatory neutrophil and T cell recruitment accompanied by increased expression of tubular injury genes and a decreased proportion of differentiated tubules. Depletion of neutrophils and T cells after day 5 reduced tubular cell loss and associated kidney atrophy. In kidney biopsies from patients with acute kidney injury, T cell and neutrophil numbers negatively correlated with recovery of estimated glomerular filtration rate. Together, our findings demonstrate that macrophage persistence after injury promotes a T cell- and neutrophil-mediated proinflammatory milieu and progressive tubule damage. Acute kidney injury can lead to chronic kidney disease. Here the authors show that the transition is related to a macrophage-mediated second wave of inflammatory cells that promote late tubule injury, dedifferentiation and fibrosis. Suppressing this second wave reduced tubular loss and kidney atrophy.

| S-EPMC9391331 | biostudies-literature

Single cell RNA-seq analyses of kidney repair and how maladaptive repair leads to kidney atrophy following ischemia/reperfusion injury

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.

2021-02-03 | GSE161758 | GEO

Single cell profiling in COVID-19 associated acute kidney injury reveals patterns of tubule injury and repair in human

Project description:The cellular mechanisms of kidney tubule repair are poorly characterized in human. Here, we applied single-cell RNA sequencing to analyze the kidney in the first days after acute injury in 5 patients with severe COVID19. We found that tubule repair follows two converging patterns involving the plasticity of mature tubule cells and the expansion and differentiation of progenitor-like cells. Tubule repair by cell plasticity displayed substantial similarities between mouse and man and determined the transient expansion of undifferentiated tubule cells with altered functional and metabolic properties. Progenitor-like cells marked by PROM1 proliferated in response to injury and followed a differentiation process characterized by the sequential activation of the WNT, NOTCH and HIPPO signaling pathways. Taken together, our analyses reveal cell state transitions and fundamental cellular hierarchies underlying kidney injury and repair in patients.

2024-01-30 | GSE185778 | GEO

Effect of GW4064 on primary cultured mouse kidney proximal tubule cells

Project description:Global gene expression in the primary cultured mouse kidney proximal tubule cells treated either DMSO or 1uM GW4064 (a FXR agonist) was compared. Results provide insight into mechanisms underlying effects of FXR activation on gene expression in mouse kidney proximal tubule cells. Male C57/BJ mice aged 6 weeks were sacrificed under anesthesia and kidney proximal tubule cells were cultured until confluent. Cells were treated with either GW4064 (1uM) or equal amount of DMSO and incubated for 24 hours. 4 total RNA samples per group were analyzed and gene expression was compared between the groups.

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Translational profiling of proximal tubule in fibrotic kidney

Project description:Injury to the proximal tubule plays a central role in the initiation and progression of kidney fibrosis, and rates of chronic kidney disease progresses approximately 50% faster in males compared to females. We applied Translating Ribosome Affinity Purification (TRAP) followed by RNA-sequencing to characterize the cell-specific proximal tubule transcriptional landscape during fibrosis in male vs. female mice.

2019-09-21 | GSE125015 | GEO

VCAM-1 mediates proximal tubule-immune cell cross talk in failed tubule recovery during AKI-to-CKD transition

Project description:Studies in animal models have suggested a linkage between the inflammatory response to injury and subsequent nephron loss during the acute kidney injury (AKI) to chronic kidney disease (CKD) transition. Failure of normal repair during the CKD transition correlates with de novo expression of vascular cell adhesion protein-1 (VCAM-1) by a subset of injured proximal tubule cells. This study identified the role of VCAM-1 expression in promoting the failed repair state. Single-cell transcriptome analysis of patients with AKI and CKD and whole kidney RNA and protein analyses of mouse models of CKD confirmed a marked increase of VCAM-1 expression in the proximal tubules of injured kidneys. In immortalized mouse proximal tubular cells and primary cultured renal cells (PCRCs), VCAM-1 expression was induced by proinflammatory cytokines including tumor necrosis factor (TNF)-α and interleukin (IL)-1β. Analyses of bulk RNA sequencing of TNF-α-treated primary cultured renal cells or pseudo-bulk RNA sequencing of biopsies from Kidney Precision Medicine Project datasets indicated activation of NF-κB and an enrichment of inflammatory response and cell adhesion pathways in VCAM-1-positive cells. Pharmacological inhibition of NF-κB signaling or genetic deletion of myeloid differentiation factor 88 and TIR domain-containing adapter-inducing interferon-β suppressed TNF-α- and IL-1β-induced VCAM-1 expression in vitro. TNF-α stimulation or overexpression of VCAM-1 significantly increased splenocyte adhesion to the mouse proximal tubular monolayer in culture. These results demonstrate that persistence of proinflammatory cytokines after AKI can induce NF-κB-dependent VCAM-1 expression by proximal tubule cells, mediating increased immune cell adhesion to the tubule and thus promoting further tubule injury and greater risk of progression from AKI to CKD.

2024-09-03 | GSE254359 | GEO

Effect of GW4064 on primary cultured mouse kidney proximal tubule cells

Project description:Global gene expression in primary cultured mouse kidney proximal tubule cells treated with either DMSO or 1uM GW4064 (an FXR agonist) was compared. Results provide insight into mechanisms underlying effects of FXR activation on gene expression in mouse kidney proximal tubule cells.

2015-06-26 | GSE70296 | GEO

Single-nuclear transcriptomics reveals a diversity of proximal tubule cell states in a dynamic response to acute kidney injury.

Project description:We performed a mild-to-moderate ischemia reperfusion injury (IRI) to model injury responses reflective of kidney injury in a variety of clinical settings. Single-nuclear RNA-sequencing (snRNA-seq) of genetically labeled injured PTCs at 7-days (“early”) and 28-days (“late”) time points post-IRI identified specific gene and pathway activity in the injury-repair transition. In particular, we identified Vcam1+/Ccl2+ proximal tubule cells at a late injury stage distinguished by marked activation of NF-kB-, TNF- and AP-1-signaling pathways. This population of PTCs showed features of a senescence-associated secretory phenotype but did not exhibit G2/M cell cycle arrest. These pro-inflammatory, pro-fibrotic proximal tubule cells are likely triggers for chronic disease progression.

2021-06-16 | GSE171417 | GEO

TGFß1-driven epithelial to mesenchymal transition in human kidney cell line

Project description:TGFbeta is the major cytokine driver of fibrosis in the kidney and other tissue. Epithelial-mesenchymal transition has been postulated to contibrute to renal fibrosis in diseases such as diabetic nephropathy. We wished to identify novel genes that were upregulated in human kidney epithelial cells in response to TGFb1.The transcriptional responses for human proximal tubule epithelial cells to 10 ng/ml TGFbeta1 was examined over 24 and 48 hr There were three treatment groups: vehicle, 24hr TGFb1, 48 hr TGFb1. Each treatment was carried out in triplicate 10 cm plates and the experiment was carried out in triplicate using consecutive passages of cells.

2011-05-30 | E-GEOD-23338 | biostudies-arrayexpress

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