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Single-cell RNA Sequencing of Wild Type and Cisplatin Induced AKI (3d and 7d groups) Mouse Kidney

ABSTRACT: Purpose: By using single-cell RNA sequencing to reveal the heterogeneity and dynamic variation of immune cell subsets in kidney injury and repairment phases Methods: 10×Genomic single-cell RNA sequencing at Sham, day 3 and day 7 time points of murine model of cisplatin induced AKI were conducted to distinguish cell subsets according to transcriptomic profile and displayed dynamic changes during acute inflammation and resolution of renal injury Results: In total, over 150.2 Gb clean reads were produced. A single-cell atlas of 36 clusters (11 cell types) of murine kidneys were generated and revealed marked changes in the proportion and gene expression of macrophage (MΦ) and proximal tubular (PT) cell subsets during injury and repair. Novel resident-MΦ cluster (Cx3cr1+Mki67+ MΦ) and PT cell cluster (repairing PT) with obvious proliferation potential were identified Conclusions: Macrophage took the dominant proportion in immune cells, displayed significant heterogeneity and experienced dramatic subpopulation replacement during the progression and regression stages of cis-AKI

ORGANISM(S): Mus musculus

PROVIDER: GSE179807 | GEO | 2026/07/01

REPOSITORIES: GEO

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Project description:Microarray analysis of human kidneys with acute kidney injury (AKI) has been limited because such kidneys are seldom biopsied. However, all kidney transplants experience AKI, and early kidney transplants without rejection are an excellent model for human AKI: they are screened to exclude chronic kidney disease, frequently biopsied, and have extensive follow-up. We used histopathology and microarrays to compare indication biopsies from 28 transplants with AKI to 11 pristine protocol biopsies of stable transplants. Kidneys with AKI showed increased expression of 394 injury-repair response associated transcripts, including many known epithelial injury molecules (e.g. ITGB6, LCN2), tissue remodeling molecules (e.g. VCAN), and inflammation molecules (S100A8, ITGB3). Many other genes also predict the phenotype, depending on statistical filtering rules, including AKI biomarkers as HAVCR1 and IL18. Most mouse orthologs of the top injury-repair transcripts were increased in published mouse AKI models. Pathway analysis of the injury-repair transcripts revealed similarities to cancer, development, and cell movement. The injury-repair transcript score AKI kidneys correlated with reduced function, future recovery, brain death, and need for dialysis, but not future graft loss. In contrast, histologic features of "acute tubular injury" did not correlate with function or with the molecular changes. Thus the injury-repair associated transcripts represent a massive coordinate injury-repair response of kidney parenchyma to AKI, similar to mouse AKI models, and provide an objective measure for assessing the severity of AKI in kidney biopsies and validation for the use of many AKI biomarkers. AKI biopsies sample names and CEL files are from GSE21374. All consenting renal transplant patients undergoing biopsies for cause as standard of care between 09/2004 and 10/2007 at the university of Alberta or between 11/2006 and 02/2007 at the University of Illinois were included in the analysis. In addition to the cores required for standard histopathology, we collected one core for gene expression studies. the relationship between gene expression in the biopsy and subsequent graft loss was analyzed. This dataset is part of the TransQST collection.

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Single-cell RNA Sequencing of Wild Type and Cisplatin Induced AKI (3d and 7d groups) Mouse Kidney

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