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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_2]

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_2]

PROVIDER: PRJNA1063646 | ENA |

REPOSITORIES: ENA

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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_2]

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.

2025-01-01 | GSE253008 | GEO

2025-01-01 | GSE253007 | GEO

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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| PRJNA1063645 | 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.

2022-08-14 | GSE211021 | 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

miRNome changes in the mouse kidney after unilateral ischemia-reperfusion injury and delayed contralateral nephrectomy

Project description:Comparing the effect of unilateral ischemia-reperfusion injury (IRI) or sham operation (sIRI) with delayed contralateral nephrectomy (Nx) or sham operation (sNx) in mouse kidney. IRI was performed on day 0 and the contralateral kidney was removed on day 7. Mice were sacrificed on day 8. Four animals were selected from the sham IRI-sham Nx and sham IRI-Nx groups and six animals were selected from the IRI-sham Nx and IRI-Nx groups for miRNA microArray analysis on the base of their proinflammatory (TNF-α and IL-6 and CCL2) and immune system-related (Complement component 3) mRNA expression levels.

2020-09-01 | GSE157221 | GEO

Strategic timing of contralateral nephrectomy after ischemic AKI prevents CKD by enhancing epithelial progenitor proliferation while attenuating polyploidization

Project description:Kidneys have a limited ability to self-repair, and their response to injury not seldomly leads to chronic kidney disease (CKD). An intriguing phenomenon of successful recovery is observed in models of unilateral acute kidney injury (AKI) upon contralateral nephrectomy. Here we aimed to better understand the cellular mechanisms of this enhanced reparative effect.In a time-course study with different nephrectomy delay times, we found that the most effective rescue after injury was observed when contralateral nephrectomy was performed early during AKI in both rats and mice. This timely intervention led to full functional recovery and attenuation of tubular atrophy, fibrosis, and inflammation, averting AKI-to-CKD transition. Morphometry of histopathology using pathomics revealed distinct trajectories of structural alterations of kidney tubules, distinguishing between atrophy and repair, as adaptive signatures. These responses were corroborated by transcriptomics analysis, which indicated improved cellular energy metabolism after nephrectomy. Lineage tracing of tubular progenitor cells showed that nephrectomy robustly stimulated their clonal expansion, surpassing the levels observed during spontaneous self-repair. Live cell cycle/DNA-content analysis of tubular cells demonstrated a robust polyploid response immediately after the ischemic insult, and revealed that nephrectomy attenuated long term tubular cell polyploidization, a contributor to CKD. Altogether, our data revealed that early timing of nephrectomy in experimental AKI induces an efficient repair response, involving tubular epithelial regeneration while counteracting the progression towards CKD.

2024-12-31 | GSE268009 | GEO

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