Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA392328 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5767270_1.fastq.gz | Fastqsanger.gz | |||
| SRR5767270_2.fastq.gz | Fastqsanger.gz | |||
| SRR5767265_1.fastq.gz | Fastqsanger.gz | |||
| SRR5767265_2.fastq.gz | Fastqsanger.gz | |||
| SRR5767266_1.fastq.gz | Fastqsanger.gz |
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Project description:Transcriptome sequencing identified RNAs associated with renal fibrosis in UUO rat model (urine)
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Project description:Transcriptome sequencing identified RNAs associated with renal fibrosis in UUO rat model
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Project description:Renal fibrosis is the final common pathway for chronic kidney disease. However, the detailed mechanisms and therapeutic strategies for renal fibrosis have not been established. MicroRNAs (miRNAs) are small, non coding RNAs that regulate various pathological conditions and diseases. Previous studies reported that miRNAs play a pivotal role in renal fibrosis. However, the role of miRNAs in renal fibrosis has not been completely elucidated. Therefore, in this study, miRNAs on renal fibrosis was investigated in a renal fibrosis mouse model generated by unilateral ureteral obstruction. MiRNA microarray analysis revealed 109 miRNAs that were upregulated more than 2 fold and 113 miRNAs that were downregulated less than 0.5 fold in the kidney of UUO mice compared with control mice.
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Project description:Renal fibrosis mRNA classifier: validation in experimental lithium-induced interstitial fibrosis in the rat kidney
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Project description:Renal fibrosis (RF) is the common pathological outcome and central treatment target of multiple chronic kidney diseases. Currently, the molecular mechanisms of RF remain poorly understood. Therefore, this study aimed to established the adenine- and UUO-induced rat models, identified differentially expressed genes in their renal tissues using RNA-Seq analysis, and screened RF-related hub targets and key pathways.
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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:We created a rat renal congestion model and investigated the effect of renal congestion on hemodynamics and molecular mechanisms. The inferior vena cava (IVC) between the renal veins was ligated by suture in male Sprague-Dawley rats to increase upstream IVC pressure and induce congestion in the left kidney only. Left kidney congestion reduced renal blood flow, glomerular filtration rate, and increased renal interstitial hydrostatic pressure. Tubulointerstitial and glomerular injury and medullary thick ascending limb hypoxia were observed only in the congestive kidneys. Molecules related to extracellular matrix expansion, tubular injury, and focal adhesion were upregulated in microarray analysis. Renal decapsulation ameliorated the tubulointerstitial injury. Electron microscopy captured pericyte detachment in the congestive kidneys. Transgelin and platelet-derived growth factor receptors, as indicators of pericyte-myofibroblast transition, were upregulated in the pericytes and the adjacent interstitium. With the compression of the peritubular capillaries and tubules, hypoxia and physical stress induce pericyte detachment, which could result in extracellular matrix expansion and tubular injury in renal congestion.
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Project description:Renal fibrosis is a widely used pathological indicator of progressive chronic kidney disease (CKD), and renal fibrosis mediates most progressive renal diseases as a final pathway. Nevertheless, the key genes related to the host response are still unclear. In this study, the potential gene network, signaling pathways, and key genes under UUO model in mouse kidneys were investigated by integrating two transcriptional data profiles.
2023-01-06 | GSE217654 | GEO
Project description:Renal fibrosis is a widely used pathological indicator of progressive chronic kidney disease (CKD), and renal fibrosis mediates most progressive renal diseases as a final pathway. Nevertheless, the key genes related to the host response are still unclear. In this study, the potential gene network, signaling pathways, and key genes under UUO model in mouse kidneys were investigated by integrating two transcriptional data profiles.
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Project description:Renal fibrosis is a common consequence of various progressive nephropathies, including obstructive nephropathy, and ultimately leads to kidney failure. Infiltration of inflammatory cells is a prominent feature of renal injury after draining blockages from the kidney, and correlates closely with the development of renal fibrosis. However, the underlying molecular mechanism behind the promotion of renal fibrosis by inflammatory cells remains unclear. Herein, we showed that unilateral ureteral obstruction (UUO) induced Gasdermin D (GSDMD) activation in neutrophils, abundant neutrophil extracellular traps (NETs) formation and macrophage-to-myofibroblast transition (MMT) characterized by α-smooth muscle actin (α-SMA) expression in macrophages. Gsdmd deletion significantly reduced infiltration of inflammatory cells in the kidneys and inhibited NETs formation, MMT and thereby renal fibrosis. Chimera studies confirmed that Gsdmd deletion in bone marrow-derived cells, instead of renal parenchymal cells, provided protection against renal fibrosis. Further, specific deletion of Gsdmd in neutrophils instead of macrophages protected the kidney from undergoing fibrosis after UUO. Single-cell RNA sequencing identified robust crosstalk between neutrophils and macrophages. In vitro, GSDMD-dependent NETs triggered p65 translocation to the nucleus, which boosted the production of inflammatory cytokines and α-SMA expression in macrophages by activating TGF-β1/Smad pathway. In addition, we demonstrated that caspase-11, that could cleave GSDMD, was required for NETs formation and renal fibrosis after UUO. Collectively, our findings demonstrate that caspase-11/GSDMD-dependent NETs promote renal fibrosis by facilitating inflammation and MMT, therefore highlighting the role and mechanisms of NETs in renal fibrosis.
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