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ABSTRACT: the renal pelvis urobiome in the unilateral kidney stone patients

PROVIDER: PRJNA843211 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19501700_1.fastq.gz	Fastqsanger.gz
	SRR19501700_2.fastq.gz	Fastqsanger.gz
	SRR19501637_1.fastq.gz	Fastqsanger.gz
	SRR19501637_2.fastq.gz	Fastqsanger.gz
	SRR19501638_1.fastq.gz	Fastqsanger.gz

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Single-nucleus atlas of the human kidney papilla identifies significant immune injury in patients with stone disease

Project description:Kidney stone disease causes significant morbidity and increases health care utilization. In this dataset, we applied a single-nucleus assay to renal papila samples in order to charachterize the cellular and molecular niches in patients with calcium oxalate (CaOx) stone disease and healthy subjects. In addition to identifying cell types important in papillary physiology, we characterize collecting duct cell subtypes and an undifferentiated epithelial cell type that was more prevalent in stone patients. Despite the focal nature of mineral deposition in nephrolithiasis, we uncover a global injury signature characterized by immune activation, oxidative stress and extracellular matrix remodeling. We also identify the association of MMP7 and MMP9 expression with stone disease and mineral deposition, respectively. MMP7 and MMP9 are significantly increased in the urine of patients with CaOx stone disease, and their levels correlate with disease activity. Our results define the spatial molecular landscape and specific pathways contributing to stone-mediated injury in the human papilla and identify associated urinary biomarkers.

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Project description:Urinary microbiome of pelvis urine from CaOx stone patients

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Gene Expression of Kidney from HSRA-S (congenital solitary kidney) and HSRA-C (two-kidney) using Rat Gene 1.1 ST Array [RaGene-1_1-st]

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Project description:Progressive renal disease is the consequence of destructive fibrosis. Renal fibrosis is a common outcome of many chronic kidney diseases, including diabetic kidney disease (DKD). Transforming growth factor-β1 (TGFβ1) has been identified as a major pathogenic factor underlying the development of DKD. It had been reported that the expression of miR-92b-3p had been reported to be reduced in the kidneys from diabetic mice and patients with DKD. However, the role of miR-92b-3p in the progress of renal fibrosis was remaining largely unknown. This study investigated the role of miR-92b-3p in the progression of renal fibrosis in unilateral ureteral occlusion (UUO) and unilateral ischemia-reperfusion injury (uIRI) mouse models, as well as explored its underlying mechanisms in human proximal tubular epithelial (HK2) cells. We found that renal fibrosis increased in UUO mice after miR-92b knockout, while reduced in miR-92b overexpressing mice. MiR-92b knockout aggravated renal fibrosis in unilateral ischemia-reperfusion injury. RNA-sequencing analysis, the luciferase reporter assay, qPCR analysis, and western blotting confirmed that miR-92b-3p directly targeted TGF-β receptor 1 (TGFBR1), thereby ameliorating renal fibrosis by suppressing the TGF-β/SMAD3 signaling pathway. Furthermore, we found that TGF-β suppressed miR-92b transcription through Snail family transcriptional repressors 1 (SNAI1) and SNAI2. Our results suggest that miR-92b-3p may serve as a novel therapeutic for mitigating fibrosis in chronic kidney disease.

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