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Single cell transcriptomic analysis of female mice after rhabdomyolysis-induced nephrotoxic injury

ABSTRACT: Single cell transcriptomic analysis of female mice after rhabdomyolysis-induced nephrotoxic injury

PROVIDER: PRJNA972752 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24572245_1.fastq.gz	Fastqsanger.gz
	SRR24572245_2.fastq.gz	Fastqsanger.gz
	SRR24572246_1.fastq.gz	Fastqsanger.gz
	SRR24572246_2.fastq.gz	Fastqsanger.gz
	SRR24572247_1.fastq.gz	Fastqsanger.gz

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Single cell transcriptomic analysis of female mice after rhabdomyolysis-induced nephrotoxic injury

Project description:We found that PTC undergo polyploidization immediately after glycerol-induced rhabdomyolysis (nephrotoxic-AKI). Polyploidization of PTC is controlled by YAP1. Block of YAP1 related polyploidization of TC employing a specific inhibitor of YAP1 transcriptional activity (CA3) after the acute phase of damage prevented CKD progression after AKI. To identify novel pathways and potential targets involved in AKI response and subsequent CKD development, we generated single-cell RNA sequencing (scRNAseq) datasets from nephrotoxic-AKI female mice treated with vehicle or CA3 starting from 4 days after AKI. Mice were sacrificed two weeks after AKI, when blood urea nitrogen levels, that reflect kidney functionality, were found to start diverging between treated and control mice, but before CKD development.

2024-11-01 | GSE232576 | GEO

The effect of circulating Klotho in response to nephrotoxic serum (NTS)-induced injury

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Comparison of the transcriptomic profiles of WT and complement C3-deficient mice with rhabdomyolysis-induced acute kidney injury

Project description:Rhabdomyolysis is a severe condition caused by skeletal muscle damage, leading to acute kidney injury (AKI). We demonstrate that complement has a direct pathogenic role in rhabdomyolysis-induced AKI. Deposition of C3d in the tubules of patients and mice correlated with rhabdomyolysis-induced AKI. Moreover, C3-defiient mice with rhabdomyolysis had preserved renal function. Mechanistically, C3-deficiency attenuated strongly inflammatory and apoptotic components of the renal transcriptome, perturbed by rhabdomyolysis. Complement was activated intrarenal by the lectin pathway via collectin-11. It proceeded in a C4-bypass manner and was amplified by heme-activated alternative pathway. Therefore, complement and heme are promising therapeutic targets for rhabdomyolysis-induced AKI.

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RNAseq of kidneys from a mice model of chronic leptospirosis infection and induced a secondary nephrotoxic injury by adenine feeding

Project description:Background The mysterious chronic kidney disease is multifactorial causes. One of the risk factors is leptospirosis, a re-emerging infectious disease caused by Leptospira spp., for endemic leptospirosis tend to coincide with high-incidence regions of chronic kidney disease of unknown etiology. This study aims to investigate the role of leptospirosis as an emerging culprit in which chronic subclinical kidney injury, may predispose to progressive kidney disease when superimposed on secondary nephrotoxic injury. Methods Adenine-induced renal injury in chronic leptospira-infected C57/BL6 mice were studied for evaluating the renal function, histology and gene expression changes. We employed RNA sequencing-based renal transcriptome to investigate pathogenic pathways associated with secondary nephrotoxic injury in chronic kidney injury due to leptospirosis. Results The severity of kidney lesions was increased and the expression of immune/inflammation/fibrosis genes were significantly up-regulated in either low-dose (0.1%) and high-dose (0.2%) adenine-induced renal injury superimposed on infected mice. Whole renal transcriptome analysis reveals that the substantial amplification of the tremendous amount of expressed genes and fibrosis-related pathways was found in adenine-induced kidney injury add-on to leptospira-infected mice which correlated with kidney dysfunction and fibrosis compared to infection or adenine itself. A total of 41 differentially expressed genes associated with fibrosis were identified in infected mice fed with adenine, suggesting that these potential genes contributed to aggravated renal progression occurred in adenine-fed chronic leptospira-infected mice. Conclusions In summary, this study indicates that chronic subclinical kidney infection when exposed to different degree of secondary nephrotoxic injury may predispose to exacerbated and progressive chronic kidney disease.

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Project description:Transcriptomic analysis of rhabdomyolysis induced kidney injury

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Project description:Acute kidney injury (AKI) represents a syndrome seldom characterized by a single, distinct pathophysiological cause. Rhabdomyolysis-induced acute kidney injury (RIAKI) constitutes roughly 15% of AKI cases, yet its underlying pathophysiology remains poorly understood. Using a murine model of RIAKI induced by muscular glycerol injection, we aimed to analyse transcriptomic alterations by RNAseq.

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