Ontology highlight
ABSTRACT:
PROVIDER: PRJNA899342 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In this study, we employed high-throughput RNA sequencing (RNA-Seq) to identify the Smad3-dependent lncRNAs related to renal inflammation and fibrosis in Smad3 knockout (KO) mouse models of unilateral ureteral obstructive nephropathy (UUO) and immunologically-induced anti-glomerular basement membrane glomerulonephritis (anti-GBM GN). 12 kidney tissue samples of Smad3 KO/WT mice from normal control, UUO at day 5 or anti-GBM GN at day 10 models (n=2 in each group) for whole transcriptome RNA-sequencing.
2014-03-26 | E-GEOD-55808 | 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:Small RNA sequencing of sorted cell type, mice kidneys, after unilateral ureteral obstructive (UUO) surgery after 2 days, 7 days and a reversible (rUUO) 14 day model with corresponding sham operated mice. The goal of the study is to identify micro-RNA dysregulation of expression between different cell types corresponding with kidney injury, in order to identify and assess biomarkers which could be translated into the clinical setting.
2021-01-26 | GSE150035 | 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:RNA sequencing of sorted cell types, isolated from mice kidneys, after unilateral ureteral obstructive (UUO) surgery after 2 days, 7 days and a reversible (rUUO) 14 day model with corresponding sham operated mice. The goal of the study was to identify temporal gene expression changes in different cell types corresponding with kidney injury, in order to understand cell specific transcriptomic changes in the context of kidney injury and repair.
2025-03-27 | GSE262799 | GEO
Project description:To understand the roles and mechanisms of stromal vascular fraction (SVF) in renal fibrosis induced by unilateral ureteral obstruction (UUO), we performed RNA sequencing of UUO kidneys from PBS- or SVF-treated mice. The transcriptome analysis revealed that SVF triggered significant metabolic reprogramming and improved mitochondrial function. Moreover, SVF treatment inhibited kidney inflammation as revealed by the downregulation of immune cell migration pathway. Furthermore, SVF contributed to the activation of PPAR signaling while inhibited TGF-beta signaling pathway.
2025-05-05 | GSE281130 | GEO
Project description:Kidney fibrosis is a major hallmark of chronic kidney disease and is defined by an excessive accumulation of extracellular matrix, primarily collagens. While collagen synthesis has been extensively investigated, the contribution of impaired collagen degradation to the development of fibrosis remains poorly understood. Collagen degradation involves the activity of proteases producing collagen-derived peptides (CDPs). Here we tested the hypothesis whether reduced collagen degradation participates to the development of kidney fibrosis. For that, CDPs were quantified in pelvic urine of kidney undergoing fibrosis following unilateral ureteral obstruction (UUO). C57Bl6 male mice underwent UUO- or sham-surgery and were sacrificed after 3- or 7-days (3D or 7D). Fibrosis was evaluated by histology. Urinary CDP composition (qualitative-sequences and quantitative-abundances) was analysed by mass spectrometry (MS). Based on collagen protein deposition, UUO-induced fibrosis was detected at 7D and not at 3D. At both 3D and 7D, of the more than 300 significantly different CDPs were found in UUO-pelvic urine, 70% of them displaying a reduced abundance in UUO compared to sham-bladder. In UUO-bladder urine, significant CDPs were found only at 7D with 79% of them displaying increased abundance. CDPs derived from Col1a1, Col1a2 and Col3a1 were the most represented and distributed in clusters along their parental protein sequence. Most clusters were composed of seemingly decreasing length CDPs containing the entire sequence of the shortest CDP. Within the clusters, inter-CDP correlations of abundance were very different between UUO-pelvis and UUO-bladder at 3D and 7D post-UUO. In conclusion, using a mouse model of fibrosis that enables the specific study of CDPs from the fibrotic kidney, we observe that reduced collagen degradation could play a key role in the early stages of fibrosis development. Our research suggests a potential need for a shift in the development of anti-fibrotic strategies, emphasizing not only the inhibition of collagen synthesis but also the enhancement of its degradation.
2026-01-12 | PXD064569 | Pride
Project description:In this study, adult virgin female BALB/C mice were kidney and lungs were harvested for RNA extraction (healthy kidney and lung). Adult virgin female BALB/C mice were subjected to unilateral ureter obstruction (UUO) to induce kidney fibrosis and the fibrotic kidney was harvested for RNA extraction. Adult virgin female BALB/C mice were subjected to intratracheal administration of bleomycine to induce lung fibrosis and the fibrotic lungs was harvested for RNA extraction.
2020-04-07 | GSE97546 | 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