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Identification of mechanistic chronic kidney disease biomarkers by comprehensive bulk RNA-seq transcriptomics and SWATH proteomics of the rat sub-total nephrectomy model of kidney fibrosis [RNA-Seq_1]

ABSTRACT: Identification of mechanistic chronic kidney disease biomarkers by comprehensive bulk RNA-seq transcriptomics and SWATH proteomics of the rat sub-total nephrectomy model of kidney fibrosis [RNA-Seq_1]

PROVIDER: PRJNA1063645 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27533966_1.fastq.gz	Fastqsanger.gz
	SRR27533966_2.fastq.gz	Fastqsanger.gz
	SRR27533967_1.fastq.gz	Fastqsanger.gz
	SRR27533967_2.fastq.gz	Fastqsanger.gz
	SRR27533968_1.fastq.gz	Fastqsanger.gz

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Identification of mechanistic chronic kidney disease biomarkers by comprehensive bulk RNA-seq transcriptomics and SWATH proteomics of the rat sub-total nephrectomy model of kidney fibrosis [RNA-Seq_1]

Project description:The rat sub-total nephrectomy (SNx) is a functional model of chronic kidney disease (CKD), where the main pathological driver is glomerular hypertension. Comprehensive transcriptomics and proteomics analyses on the rat SNx model were performed to identify biomarkers in plasma or urine that correlate with kidney disease and functional kidney loss. Kidneys were subjected to collagen I and III staining for fibrosis scoring, SWATH proteomics and bulk RNA-sequencing transcriptomics (RNA-seq), with SWATH also performed on plasma and urine. Differential expression analysis demonstrated significant dysregulation of genes and proteins involved in fibrosis, metabolism, and immune response in the SNx rats compared to controls. Gene ontology analysis of the intersecting genes and proteins from both studies demonstrated common biology between animal cohorts that reached the predefined kidney disease thresholds (serum creatinine >2-fold or proteinuria >3-fold increase over sham-operated). Thirteen significantly differential molecules were detected with consistent directional changes in both transcriptomics and proteomics datasets. These molecules were detected independently in kidney (both RNA and protein) and urine (protein only), but not in plasma. The bioinformatics analysis enabled the identification of mechanistic CKD biomarkers including lumican and collagen alpha-1(III) chain, whose co-expression has previously been both implicated in fibrosis and detected in urine in CKD patients.

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2025-01-01 | GSE253008 | GEO

Identification of mechanistic chronic kidney disease biomarkers by comprehensive bulk RNA-seq transcriptomics and SWATH proteomics of the rat sub-total nephrectomy (SNx) model of kidney fibrosis

Project description:The rat sub-total nephrectomy (SNx) is a functional model of chronic kidney disease (CKD), where the main pathological driver is glomerular hypertension. Comprehensive transcriptomics and proteomics analyses on the rat SNx model were performed to identify biomarkers in plasma or urine that correlate with kidney disease and functional kidney loss. SWATH proteomics and bulk RNA-sequencing transcriptomics (RNA-seq), with SWATH also performed on plasma and urine. Differential expression analysis demonstrated significant dysregulation of genes and proteins involved in fibrosis, metabolism, and immune response in the SNx rats compared to controls. Gene ontology analysis of the intersecting genes and proteins from both studies demonstrated common biology between animal cohorts that reached the predefined kidney disease thresholds (serum creatinine >2-fold or proteinuria >3-fold increase over sham-operated). About a dozen significantly differential molecules were detected with consistent directional changes in both transcriptomics and proteomics datasets. These molecules were detected independently in kidney (both RNA and protein) and urine (protein only), but not in plasma. The bioinformatics analysis enabled the identification of mechanistic CKD biomarkers whose co-expression have previously been both implicated in fibrosis and detected in urine in CKD patients.

2025-04-25 | PXD048564 | Pride

Identification of mechanistic chronic kidney disease biomarkers by comprehensive bulk RNA-seq transcriptomics and SWATH proteomics of the rat sub-total nephrectomy model of kidney fibrosis

Project description:Identification of mechanistic chronic kidney disease biomarkers by comprehensive bulk RNA-seq transcriptomics and SWATH proteomics of the rat sub-total nephrectomy model of kidney fibrosis

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| PRJNA1063646 | ENA

Transcriptomic changes in response to 5/6 or 1/3 nephrectomy

Project description:We report the changes in kidney mRNA abundance in response to 5/6 nephrectomy or 1/3 nephrectomy surgery when compared to sham operated controls.

2022-03-01 | GSE194367 | GEO

Transcriptome Changes of Microdissected Kidney Tubules triggered by Unilateral Nephrectomy [RNA-seq]

Project description:Purpose: Experiments were done in mice undergoing unilateral nephrectomy (UNx) and sham nephrectomy. At specific time points (24 hours and 72 hours) after surgery, the earliest first portion of the kidney proximal tubule (PT-S1) and the cortical collecting duct (CCD) were manually micro-dissected and utilized for transcriptomic analysis by single-tubule small sample RNA-Seq. Methods: We carried out RNA-sequencing in microdissected ealiest portion of proximal tubules (PT-S1) or cortical collecting duct (CCD) from mice with or without (sham) unilateral nephrectomy (UNx). Each group (Sham or UNx) has 3-5 biological replicates. Results and conclusion: RNA-Seq in microdissected PT-S1 at 24 hours showed that peroxisome proliferator-activated receptor alpha (PPARα) target genes were strongly upregulated. RNA-Seq in microdissected PT-S1 at 72 hours showed that cell cycle related genes were strongly upregulated. RNA-Seq in microdissected CCD at both 24 hours and 72 hours showed that cell cycle related genes were strongly upregulated.

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Single-nuclei RNA/ATAC-seq of healthy and injured human kidney nephrectomy tissue

Project description:Improved understanding of the renal cell phenotypes and intercellular signaling pathways that mediate chronic kidney disease is required to develop novel therapeutics. To this end, we performed simultaneous single nuclear RNA and ATAC-sequencing on kidney tissue from patients undergoing tumour nephrectomy, where the ureter was either obstructed by tumour or remained unobstructed. In obstructed kidneys a discrete subset of proximal and ascending thin limb of loop of Henle tubular cells acquired a pro-inflammatory phenotype enriched in senescence markers.

2025-03-25 | GSE254185 | GEO

Investigation of Resistant Starch effect on gut microbiome in 5/6 nephrectomy mouse model of Chronic Kidney Disease

Project description:Background. Resistant Starch (RS) improves CKD outcomes. In this report we study how RS modulates host-microbiome interactions in CKD by measuring changes in abundance of proteins and bacteria in the gut. In addition, we demonstrate RS-mediated reduction in CKD-induced kidney damage. Methods. Eight mice underwent 5/6 nephrectomy to induce CKD and 8 served as healthy controls. CKD and Healthy (H) groups were further split into those receiving RS (CKDRS, n=4; HRS, n=4) and those on normal diet (CKD, n=4, H, n=4). Kidney injury was evaluated by measuring BUN/creatinine and by most-mortem histopathological evaluation. Cecal contents were analyzed mass spectrometry-based metaproteomics. PEAKS Studio was used to identify peptides via de novo sequencing. A set of R/Bioconductor packages and in house written scripts was further used to infer bacteria present, to evaluate changes in proteins and bacterial abundances, and to perform statistical analysis and hierarchical clustering. Results. The 5/6 nephrectomy compromised kidney function as seen by an increase in creatinine and BUN. Representative photomicrographs of trichrome-stained kidney sections showed reduced tubulointerstitial injury in CKD mice fed HAM-RS2 diet comparing to CKD mice fed normal diet. Identified organisms and proteins point toward a higher population of butyrate-producing bacteria, and reduced abundance of mucin-degrading bacteria. Conclusion. Resistant starch slows the progression of chronic kidney disease. Gut barrier function through maintenance of the mucin barrier plays a role in RS-associated improvements in CKD phenotype. Resistant starch supplementation leads to the active bacterial proliferation and the reduction of harmful bacterial metabolites.

2020-10-19 | PXD019623 | Pride

Renal gene expression in two mouse strains with different propensity to develop chronic kidney disease after subtotal nephrectomy at different time-points

Project description:Renal gene expression analysis was performed in mouse strains with different propensity to develop progressive chronic kidney disease (CKD) after subtotal nephrectomy: the FVB strain which is spontaneously highly predisposed to CKD and the C57BL/6 which is spontaneously not predisposed to CKD. Subtotal nephrectomy (Nx) is normally initially compensated by proliferative tissue repair (2 days after nephrectomy). After this initial proliferation follows a quiescent period (28 days after NX). Finally, specifically in the sensitive strain there is lesion onset (53 days after Nx). Gene expression was monitored on RNA from whole kidneys from different mouse strains Sham operated or Nephrectomised at three different time-points.

2020-06-01 | GSE148084 | GEO

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