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Single-nucleus transcriptional profiling of chronic kidney disease after cisplatin nephrotoxicity

ABSTRACT: Single-nucleus transcriptional profiling of chronic kidney disease after cisplatin nephrotoxicity

PROVIDER: PRJNA1000910 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25473863.fastq.gz	Fastqsanger.gz
	SRR25473864.fastq.gz	Fastqsanger.gz
	SRR25473865.fastq.gz	Fastqsanger.gz
	SRR25473866.fastq.gz	Fastqsanger.gz
	SRR25473867.fastq.gz	Fastqsanger.gz

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Single-nucleus transcriptional profiling of chronic kidney disease after cisplatin nephrotoxicity

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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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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.

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