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Whole transcriptome analysis of UUO mouse model of renal fibrosis reveals new molecular players in kidney diseases

ABSTRACT: The study demontrates differences in the transcriptome ( both of protein coding transcripts and long non-coding RNAs) in the unilateral ureteric obstruction model of renal fibrosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE79443 | GEO | 2016/05/09

SECONDARY ACCESSION(S): PRJNA315860

REPOSITORIES: GEO

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Whole-transcriptome analysis of UUO mouse model of renal fibrosis reveals new molecular players in kidney diseases.

Project description:Transcriptome analysis by RNA-seq technology allows novel insights into gene expression and regulatory networks in health and disease. To better understand the molecular basis of renal fibrosis, we performed RNA-seq analysis in the Unilateral Ureteric Obstruction (UUO) mouse model. We analysed sham operated, 2- and 8-day post-ligation renal tissues. Thousands of genes with statistical significant changes in their expression were identified and classified into cellular processes and molecular pathways. Many novel protein-coding genes were identified, including critical transcription factors with important regulatory roles in other tissues and diseases. Emphasis was placed on long non-coding RNAs (lncRNAs), a class of molecular regulators of multiple and diverse cellular functions. Selected lncRNA genes were further studied and their transcriptional activity was confirmed. For three of them, their transcripts were also examined in other mouse models of nephropathies and their up- or down-regulation was found similar to the UUO model. In vitro experiments confirmed that one selected lncRNA is independent of TGF? or IL1b stimulation but can influence the expression of fibrosis-related proteins and the cellular phenotype. These data provide new information about the involvement of protein-coding and lncRNA genes in nephropathies, which can become novel diagnostic and therapeutic targets in the near future.

| S-EPMC4870569 | biostudies-literature

Proteomic profiling in mouse kidneys post-UUO

Project description:Increased export of transglutaminase-2 (TG2) by tubular epithelial cells (TECs) into the surrounding interstitium modifies the extracellular homeostatic balance leading to fibrotic membrane expansion. Although silencing of extracellular TG2 ameliorates progressive kidney scarring in animal models of chronic kidney disease, the pathway through which TG2 is secreted from TECs and contributes to disease progression has not been elucidated. In this study, we developed a global proteomic approach to identify binding partners of TG2 responsible for TG2 externalization in kidneys subjected to unilateral ureteric obstruction, using TG2-knockout kidneys as negative controls. We report a robust and unbiased analysis of the membrane interactome of TG2 in fibrotic kidneys relative to the entire proteome post-UUO detected by SWATH-mass spectrometry.

2018-02-07 | PXD008173 | Pride

Receptor Notch-3 - role in kidney fibrosis using an UUO model

Project description:Gene array of kidney tissue of wild type and Notch-3 knockout mice was performed following unilateral ureteral obstruction (UUO).

2020-12-31 | GSE156181 | GEO

Murine Kidney Tissue: Unilateral ureteral obstructed (UUO) mice vs. Sham control

Project description:Gene expression changes induced by unilateral ureteral obstruction in mice.

2018-02-23 | GSE96101 | GEO

Mouse kidney tissue: UUO-METTL3fl/fl, cre T vs. UUO-METTL3fl/fl, wt

Project description:The mRNA transcriptome and m6A methylation microarray profiling of mouse kidney tissues. Kidney tissues from the sham-operated group and unilateral ureteral ligation/obstruction (UUO) kidney tissues were compared. The latter were mainly fibrotic kidney tissues. The goal was to identify the effect of the renal fibrosis on gene expression and corresponding m6A modifications during kidney fibrosis.

2023-08-09 | GSE226506 | GEO

Mouse kidney tissue: Control vs. UUO

2023-08-09 | GSE226505 | GEO

Exploring new pathways involved during experimental renal fibrogenesis in the Unilateral Ureteral Obstruction

Project description:Chronic kidney disease (CKD) is a burden for Public Health and concerns millions of individuals worldwide. Independently of the cause, CKD is secondary to the replacement of functional renal tissue by extra-cellular matrix proteins (i.e fibrosis) that progressively impairs kidney function. The pathophysiological pathways that control the development of renal fibrosis are common to most of the nephropathies involving native kidneys or kidney grafts. Unfortunately, very few treatments are available to stop renal fibrosis and most of the therapeutic strategies are often barely able to slow down the progression of fibrogenesis in native kidneys. Therefore, it is mandatory to discover new therapeutic pathways to stop renal fibrosis. Our objective is to study new pathways involved in renal fibrosis. We thus decided to use the model of Unilateral Ureteral renal Obstruction in mice, a fast and reproducible experimental model of renal fibrosis. We studied renal fibrosis using experimental model of ureteral unilateral obstruction in mice, which was performed by complete ligation of the left ureter. The control lateral right kidney served as internal control.

2013-02-10 | E-GEOD-38117 | biostudies-arrayexpress

Effect of Hirudin,Curcumin or Buyang Huanwu Formulas Exposure on Gene Expression of UUO rats

Project description:We performed RNA-Seq analysis to investigate the gene expression patterns in the kidneys of rats with unilateral ureteral obstruction (UUO) treated with hirudin, curcumin or Buyang Huanwu Formula(BHF).

2021-08-06 | GSE181380 | GEO

Single Cell Transcriptomics reveals renal myeloid dynamics post reversable unilateral ureteric injury

Project description:The kidney has limited capacity to regenerate following injury and preferentially repairs chronic injury with secreted extracellular matrix proteins. This can be a progressive process with functioning kidney tissue being replaced detrimentally with fibrotic scar tissue, ultimately leading to kidney failure. Whilst the renal response to injury has been well described it has been examined at whole organ resolution and there has been very limited description of the contribution of individual cells to the kidney’s reparative ability. Using the reversible unilateral ureteric obstruction model, a model of reversable injury, we describe the transcriptomic changes that occur during obstructive renal injury and subsequent repair at a single cell resolution and describe the altered myeloid cell populations and kinetics likely involved in ongoing tissue repair.

2020-09-27 | GSE140023 | GEO

DsbA-L mediated renal tubulointerstitial fibrosis in UUO mice.

Project description:Recent studies have reported that upregulation of disulfide-bond A oxidoreductase-like protein (DsbA-L) prevented lipid-induced renal injury in diabetic nephropathy (DN). However, the role and regulation of proximal tubular DsbA-L for renal tubulointerstitial fibrosis (TIF) remains unclear. In current study, we found that a proximal tubules-specific DsbA-L knockout mouse (PT-DsbA-L-KO) attenuated UUO-induced TIF, renal cell apoptosis and inflammation. Mechanistically, the DsbA-L interacted with Hsp90 in mitochondria of BUMPT cells which activated the signaling of Smad3 and p53 to produce connective tissue growth factor (CTGF) and then resulted in accumulation of ECM of BUMPT cells and mouse kidney fibroblasts. In addition, the progression of TIF caused by UUO, ischemic/reperfusion (I/R), aristolochic acid, and repeated acute low-dose cisplatin was also alleviated in PT-DsbA-L-KO mice via the activation of Hsp90 /Smad3 and p53/CTGF axis. Finally, the above molecular changes were verified in the kidney biopsies from patients with obstructive nephropathy (Ob). Together, these results suggest that DsbA-L in proximal tubular cells promotes TIF via activation of the Hsp90 /Smad3 and p53/CTGF axis.

| S-EPMC7501299 | biostudies-literature

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