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Evaluation of cisplatin-induced injury in human kidney organoids

ABSTRACT: Evaluation of cisplatin-induced injury in human kidney organoids

PROVIDER: PRJNA605973 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11066831.fastq.gz	Fastqsanger.gz
	SRR11066832.fastq.gz	Fastqsanger.gz
	SRR11066833.fastq.gz	Fastqsanger.gz
	SRR11066834.fastq.gz	Fastqsanger.gz
	SRR11066835.fastq.gz	Fastqsanger.gz

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Evaluation of cisplatin-induced injury in human kidney organoids

Project description:Acute kidney injury (AKI) remains a major global healthcare problem and there is a need to develop human-based models to study AKI in vitro. Towards this goal, we have characterized induced pluripotent stem cell-derived human kidney organoids and their response to cisplatin, a chemotherapeutic drug that induces AKI and preferentially damages the proximal tubule. We found that a single treatment with 50 µM cisplatin induces HAVCR1 and CXCL8 expression, DNA damage (γH2AX) and cell death in the organoids in a dose-dependent manner but greatly impairs organoid viability. DNA damage was not specific to the proximal tubule but also affected the distal tubule and interstitial cell populations. This lack of specificity correlated with low expression of the proximal tubule-specific SLC22A2/OCT2 transporter for cisplatin. To improve viability, we developed a repeated low-dose regimen of 4x 5 µM cisplatin over 7 days and found this causing less toxicity while still inducing a robust AKI response that included secretion of known AKI biomarkers and inflammatory cytokines. This work validates the use of human kidney organoids to model aspects of AKI, with the potential to identify new AKI biomarkers and develop better therapies.

2020-02-29 | GSE145085 | GEO

Hypoxic injury triggers maladaptive repair in human kidney organoids

Project description:Reduction in blood supply to the kidneys occurs to certain extent during kidney injury (AKI). Individuals who suffered AKI are at risk of developing chronic kidney disease (CKD) through a maladaptive repair process. At present, no therapies exist to prevent the AKI to CKD transition. Here, we present a human kidney organoid model of AKI and maladaptive regeneration. Organoids were generated from human induced pluripotent stem cells and cultured in hypoxic or normoxic conditions from days 18-20 of differentiation. Organoids were collected at day 20 to assess hypoxic injury, and after a 5-day recovery in normoxic conditions to assess maladaptive repair. The transcriptome, proteome and metabolome were profiled. Gene expression analysis of day 20 hypoxic organoids identified signatures of injury, cell death (necroptosis and ferroptosis), cell cycle arrest and changes in metabolism. The maladaptive repair phenotype was supported by enrichment of pathways associated with inflammatory signals, oxidative stress, and tissue remodelling. Specific genes associated with kidney injury and disease such as GDF15, MMP7, ICAM1, TGFB1, CCN1, C3 and S100A8/9 were upregulated. Single-cell RNA sequencing localised expression of maladaptive repair genes and activation of TNF and JAK-STAT signalling pathways specific to tubular epithelial cells. Dysregulation in metabolic pathways such as glycolysis and gluconeogenesis, amino acid and lipid metabolisms were conserved in this model. Therefore, these results support the use of kidney organoids as a model of AKI and early CKD that can be used for biomarker validation, elucidation of pathological mechanisms, and drug screening.

2026-06-26 | PXD042882 | Pride

Transcriptomic dataset after cisplatin induced acute kidney injury

Project description:Cisplatin-induced acute kidney injury (AKI) is one of the most common and severe side effects and can prevent the use of this important agent. Unfortunately, preventive or therapeutic tools to address cisplatin-induced AKI are lacking. Interestingly, in the last decades a row of preconditioning strategies that employ the activation of cellular stress resistance pathways have been shown to be promising approaches to protect from organ injury in rodent models. Here, we characterized both the protective potential and the underlying molecular patterns of two strategies – caloric restriction and hypoxic preconditioning – in mice treated with cisplatin.

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Transcriptomic dataset after cisplatin induced acute kidney injury

Project description:Transcriptomic dataset after cisplatin induced acute kidney injury

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Project description:Profiling of proteolytic events mouse kidneys during cisplatin-induced kidney damage. Kidneys from vehicle-treated mice are compared to cisplatin-treated mice and cisplatin treatment in animals preconditioned by hypoxia or calory restriction regimes.

2018-10-29 | PXD007186 | Pride

Molecular Mechanisms of the Progression of Cisplatin-Induced Acute Kidney Injury to Chronic Kidney Disease

Project description:Though there has been extensive investigation of the kidney's acute cellular and molecular responses following cisplatin treatment, the mechanisms of progression from acute to chronic disease have not been explored. In this study, we use functional and morphological metrics to establish a time point when the transition from acute repairable kidney injury to chronic irreparable disease is clearly established. We then used microarray and western blot analysis to investigate the molecular changes (i.e., gene expression, pathway activity, signaling) associated with the transition from acute to chronic cisplatin-induced kidney disease.

2017-12-13 | GSE107976 | GEO

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Project description:Acute kidney injury and nephrotoxicity are important clinical side effects of cisplatin. Thus, the mechanisms of this disease, and potential treatment options are important to understand in their entity. Here, we analyzed the proteome of cisplatin induced acute kidney injury in a mouse model. Functionally we found that calorie restriction was able to completely blunt Cisplatin induced AKI, and hypoxia ameliorated cCisplatin induced AKI. To investigate the mechanism for this in high throughput, we performed label-free single-shot proteomic analyses of these kidneys.Acute kidney injury and nephrotoxicity are important clinical side effects of cisplatin. Thus, the mechanisms of this disease, and potential treatment options are important to understand in their entity. Here, we analyzed the proteome of cisplatin induced acute kidney injury in a mouse model. Functionally we found that calorie restriction was able to completely blunt Cisplatin induced AKI, and hypoxia ameliorated cCisplatin induced AKI. To investigate the mechanism for this in high throughput, we performed label-free single-shot proteomic analyses of these kidneys.

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Spatial profiling of hypoxic injury in human kidney organoids

Project description:This dataset relates to a spatial transcriptomic experiment investigating potential reparative and inflammatory roles for macrophages in human iPSC-derived kidney organoids exposed to hypoxic injury, linked to a broader study of ischaemic kidney injury and repair in this model (https://doi.org/10.1101/2023.10.04.558359). Acute kidney injury (AKI) is a common clinical disorder linked to high rates of illness and death. Ischaemia is a leading cause of AKI, where reduced blood flow to the kidney triggers hypoxia and cell death in the nephron epithelium, impairing essential fluid handling and waste removal functions. While injured tubules have some capacity to recover, severe injury can result in chronic kidney disease (CKD) through a maladaptive repair process characterised by failed epithelial regeneration, inflammation, and metabolic dysregulation. Immune cells critically influence kidney injury responses in vivo, with tissue-resident macrophages driving either repair or harmful inflammation, fibrosis, and progression to CKD. To complement prior bulk RNAseq analysis and investigate the role of macrophages in AKI and maladaptive repair within the tissue microenvironment, we integrated iPSC-derived macrophages into kidney organoids and investigated their response to hypoxic injury and effect on the surrounding tissue with spatial transcriptomics.

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Transcription profiling of rat kidney exposed to different doses of Cisplatin- ILSI-HESI NephroToxicity Study - Cisplatin

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2007-01-10 | E-TOXM-11 | biostudies-arrayexpress

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