Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33516888_1.fastq.gz | Fastqsanger.gz | |||
| SRR33516888_2.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: The goal of this study was to characterize the kidney transcriptome of Mus musculus and Acomys cahirinus after unilateral ureteral obstruction (UUO) kidney injury. Methods: Kidney mRNA-seq profiles of 10 week old mouse and spiny mouse were generated at 2 day and 5 days after unilateral ureteral obstruction injury in triplicate, using Illumina NovaSeq 6000. The sequence reads that passed quality filters were analyzed at the transcript isoform level with Salmon, edgeR and a limma-voom pipeline in R. Results: For both Mus musculus and Acomys cahirinus kidneys, we mapped about 50 million sequence reads per sample to the mouse transcriptome and identified 20580 transcripts in kidneys of Mus musculus and 54075 transcripts in the kidneys of Acomys cahirinus. Using 1.5 fold change and FDR < 0.05, number of transcripts that are significantly different between Mus musculus samples: 3915 between normal and day 2 after UUO, 5365 between normal and day 5 after UUO. For Acomys cahirinus: 1765 between normal and day 2 after UUO, 2499 between normal and day 5 after UUO. Conclusions: Our study demonstrate there were many conserved responses to kidney injury between M. musculus and A. cahirinus despite the divergent outcomes for kidney fibrosis.
2021-09-13 | GSE168876 | GEO
Project description:Label-free quantitative proteomics for mouse kidney tissue of UUO vs Sham was used for discovery of differential expressed proteins in the process of renal fibrosis. Compared to sham mice, we found that 216 upregulated proteins and 215 downregulated proteins in UUO mice according to fold change ≥ 5, adjusted-p ≤ 0.01. Then, we will study the potential mechanism according to differential expressed proteins.
2022-09-30 | PXD029310 | Pride
Project description:Renal injury leads to chronic kidney disease for which women are not only more likely to be diagnosed with than men but also have poorer outcomes as well. We have previously shown that expression of Sprr2f, a member of the Small Proline Rich Region (Sprr) gene family, is increased several hundred fold after renal injury using a unilateral ureter obstruction (UUO) mouse model. To better understand the role of Sprr2f in renal injury, we generated a Sprr2f knockout (Sprr2f-KO) mouse model using CRISPR-Cas9 technology. To identify genes that are differentially expressed in Sprrf2f-KO mice after UUO, we performed gene expression profiling by RNA-seq on kidney tissues harvested from Sprr2f-KO mice at time 0 (n=4) and after 5 days (n=3), a time known to show dramatic changes in gene expression. Compared to day 0, expression levels of 162 genes were significantly changes with 121 up-regulated and 41 down-regulated 5 days after obstruction. Enrichment analysis using PANTHER Classification System identified 12 and 2 pathways enriched in genes that are upregulated or downregulated after UUO respectively. Eleven out of the 12 pathways enriched in the genes upregulated after UUO are related to metabolism such as drug metabolic process, consistent with a profound role of kidney as a major clearance organ of the body responsible for the elimination of many xenobiotics and prescription drugs. Interestingly, the only pathway not related to metabolism enriched in genes upregulated by UUO is oxidation-reduction, suggesting a potential role of oxidative stress in renal damage after UUO in Sprr2-KO animals. This phenotype is not observed in Sprr2f-WT animals after UUO in our previous gene expression profiling study, suggesting that Sprr2f function is sufficient to protect kidney from oxidative damage after UUO in Sprr2f-WT animals.
2020-10-13 | GSE153010 | GEO
Project description:Chronic kidney disease is associated with progressive renal fibrosis, where perivascular cells give rise to the majority of α-SMA positive myofibroblasts. We sought to identify pericytic miRNAs that could serve as a target to decrease myofibroblast formation. We induced kidney fibrosis in FoxD1-GC;Z/Red-mice by unilateral ureteral obstruction (UUO) followed by FACS sorting of dsRed-positive FoxD1-derivative cells and miRNA profiling. MiR-132 selectively increased 21-fold during pericyte-to-myofibroblast formation whereas miR-132 was only 2.5-fold up in total kidney lysates (both in UUO and ischemia-reperfusion injury). MiR-132 silencing in UUO decreased collagen deposition (35%) and tubular apoptosis. Immunohistochemistry, western blot and qRT-PCR confirmed a similar decrease in interstitial α-SMA+ cells. Pathway analysis identified a rate-limiting role for miR-132 in myofibroblast proliferation that was confirmed in vitro. Indeed, antagomir-132 treated mice displayed a reduction in the number of proliferating, ki67+ interstitial myofibroblasts. Interestingly, this was selective for the interstitial compartment and did not impair the reparative proliferation of tubular epithelial cells, as evidenced by an increase in ki67+ epithelial cells, as well as increased (p-)RB1, Cyclin-A and decreased RASA1, p21 levels in kidney lysates. Taken together, silencing miR-132 counteracts the progression of renal fibrosis by selectively decreasing myofibroblast proliferation and could potentially serve as a novel antifibrotic therapy. Total RNA obtained from FACS sorted mouse renal FoxD1-derivatve interstitial cells from mice that were treated with antagomir-132 or scramblemir and underwent UUO (n=4)
2016-02-16 | E-GEOD-76548 | biostudies-arrayexpress
Project description:Cellular senescence is associated with the progression of chronic kidney disease (CKD), and accelerated tubular cell senescence promotes the pathogenesis of renal fibrosis. We established three animal models related to Chronic Kidney Disease, including aristolochic acid nephropathy (AAN), bilateral ischemia/reperfusion injury (BIRI) and unilateral ureter obstruction (UUO). By RNA sequencing analysis in AAN, BIRI and UUO mice, we observed significant changes of senescence and fibrosis related genes.
2024-02-03 | GSE254440 | GEO
Project description:Cardiorenal syndrome (CRS) type 4 is prevalent among the chronic kidney disease (CKD) population, with many patients dying from cardiovascular complications. However, limited data regarding cardiac transcriptional changes induced early by CKD is available. We used a murine unilateral ureteral obstruction (UUO) model to evaluate cardiac transcriptional regulation at 21 days post-surgery through RNA-seq and bioinformatics. UUO leads to significant kidney injury, low uremia, and pathological cardiac remodeling. RNA-seq analysis identified 76 differentially expressed genes (DEGs) in UUO hearts. Upregulated DEGs were significantly enriched in cell cycle and cell division pathways, immune responses, cardiac repair, inflammation, proliferation, oxidative stress, and apoptosis. Gene Set Enrichment Analysis further revealed mitochondrial oxidative bioenergetic pathways, autophagy, and peroxisomal pathways are downregulated in UUO hearts. Vimentin was also identified as an UUO-upregulated transcript. Our results emphasize the relevance of extensive transcriptional and epigenetic changes, mitochondrial dysfunction, homeostasis deregulation, fatty-acid metabolism alterations, and vimentin upregulation in CRS type 4 development.
2024-03-22 | GSE235751 | GEO
Project description:Mouse kidney tissue: Control vs. UUO
| PRJNA940451 | ENA
Project description:p300 was knockout in renal proximal tubule cells of mouse kidney. Mouse was sacrificed 8 days after UUO sugery
2025-04-08 | GSE271305 | GEO
Project description:Lipid mal-metabolism, particularly fatty acid oxidation (FAO) dysfunction, is a major driver of renal fibrosis. However, detailed regulatory mechanisms underlying this process remain unclear. In this study, we demonstrated that acyl-CoA thioesterase 12 (Acot12) is a key regulator of lipid metabolism in fibrotic kidneys. A significantly decreased level of ACOT12 was observed in a kidney sample of human patients with chronic kidney disease as well as in mouse kidney injury. Acot12 deficiency induces lipid accumulation and fibrosis in mice subjected to unilateral ureteral obstruction (UUO). Fenofibrate administration does not reduce renal fibrosis in Acot12-/- mice with UUO. Moreover, restoration of peroxisome proliferator-activated receptor (PPAR in Acot12-/- Ppar-/- kidneys with UUO exacerbated lipid accumulation and renal fibrosis, whereas restoration of Acot12 in Acot12-/- Ppar-/- kidneys with UUO significantly reduced lipid accumulation and renal fibrosis suggesting, mechanistically, Acot12 deficiency exacerbates renal fibrosis independently of PPAR. In Acot12-/- kidneys with UUO, a reduction in the selective autophagic degradation of peroxisomes and pexophagy with a decreased level of ACBD5 was observed. In conclusion, our study demonstrates the functional role and mechanistic details of Acot12 in the progression of renal fibrosis, provides a preclinical rationale for regulating Acot12 expression and presents a novel means of preventing renal fibrosis.
2025-03-12 | GSE261115 | GEO