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MiRNA profiling of urinary exosomes to assess the progression of acute kidney injury

ABSTRACT: miRNA profiling of urinary exosomes to assess the progression of acute kidney injury

PROVIDER: PRJNA513035 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8393800.fastq.gz	Fastqsanger.gz
	SRR8393810.fastq.gz	Fastqsanger.gz
	SRR8393820.fastq.gz	Fastqsanger.gz
	SRR8393791.fastq.gz	Fastqsanger.gz
	SRR8393801.fastq.gz	Fastqsanger.gz

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miRNA profiling of urinary exosomes to assess the progression of acute kidney injury

Project description:Using renal ischemia-reperfusion injury as a model of acute kidney injury, we deteremined temporally-released miRNAs released in urinary exosomes during the injury

2019-01-05 | GSE124669 | GEO

miRNA profiling of urinary exosomes to assess the progression of acute kidney injury

Project description:miRNA profiling of urinary exosomes to assess the progression of acute kidney injury

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miRNA profiling of urinary exosomes to assess the progression of acute kidney injury

Project description:Because exosomes have gained attention as a source of biomarkers, we investigated if miRNAs in exosomes (exo-miRs) can report the disease progression of organ injury. Using renal ischemia-reperfusion injury (IRI) as a model of acute kidney injury (AKI), we determined temporally-released exo-miRs in urine during IRI and found that these exo-miRs could reliably mirror the progression of AKI. From the longitudinal measurements of miRNA expression in kidney and urine, we found that release of exo-miRs was regulated sorting process, rather than simply representing their intracellular biosynthesis. In the injury state, miR-16, miR-24, and miR-200c were increased in the urine. Interestingly, expression of target mRNAs of these exo-miRs was significantly altered in renal medulla. Next, in the early recovery state, urinary exo-miRs (miR-9a, miR-141, miR-200a, miR-200c, miR-429), which shares Zeb1/2 as a common target mRNA, were upregulated, indicating that they reflect TGF--associated renal fibrosis. Finally, release of exo-miRs (miR-125a, miR-351) was regulated by TGF-1 and was able to differentiate the sham and IRI even after the injured kidneys were functionally recovered. Altogether, these data indicate that exo-miRs released in renal IRI are largely associated with TGF- signaling. Temporal release of exo-miRs which share targets might be a regulatory mechanism to control the disease progression of AKI.

2019-03-01 | GSE125305 | GEO

miRNA profiling of urinary exosomes to assess the progression of acute kidney injury.

Project description:Because exosomes have gained attention as a source of biomarkers, we investigated if miRNAs in exosomes (exo-miRs) can report the disease progression of organ injury. Using rat renal ischemia-reperfusion injury (IRI) as a model of acute kidney injury (AKI), we determined temporally-released exo-miRs in urine during IRI and found that these exo-miRs could reliably mirror the progression of AKI. From the longitudinal measurements of miRNA expression in kidney and urine, we found that release of exo- miRs was a regulated sorting process. In the injury state, miR-16, miR-24, and miR-200c were increased in the urine. Interestingly, expression of target mRNAs of these exo-miRs was significantly altered in renal medulla. Next, in the early recovery state, exo-miRs (miR-9a, miR-141, miR-200a, miR-200c, miR-429), which share Zeb1/2 as a common target mRNA, were upregulated together, indicating that they reflect TGF-β-associated renal fibrosis. Finally, release of exo-miRs (miR-125a, miR-351) was regulated by TGF-β1 and was able to differentiate the sham and IRI even after the injured kidneys were recovered. Altogether, these data indicate that exo-miRs released in renal IRI are associated with TGF-β signaling. Temporal release of exo-miRs which share targets might be a regulatory mechanism to control the progression of AKI.

| S-EPMC6423131 | biostudies-literature

Differential miRNA expression profiling of urinary exosomes from normo- and microalbuminuric type 1 diabetic patients

Project description:The aim of this study was to compare miRNA expression in urinary exosomes from type 1 diabetic patients with and without incipient diabetic nephropathy. Overnight urine collections were obtained from normo- and microalbuminuric type 1 diabetic patients. Urines were pre-cleared by both centrifugation and filtration, urinary exosomes were isolated by two consecutive ultracentrifugation steps and total RNA extracted. Differential miRNA profiling was performed using a Human TaqMan miRNA Array A on an 7900HT Fast Real-Time PCR System. Results showed that expression of 22 urinary exosomal miRNAs differed in incipient diabetic nephropathy. Differential qPCR miRNA profiling was performed on urinary exosomes from 2 pairs of micro/normoalbuminuric type 1 diabetic patients comparable for age, sex, diabetes duration, and tightly matched for HbA1c (1° pair: 8.1 vs. 8.1, 2° pair: 8.7 vs. 8.7). MiRNAs were considered differentially expressed if they exhibited greater than twofold expression differences in both pairs.

2014-02-14 | E-GEOD-48318 | biostudies-arrayexpress

Identifying urinary RNA as non-invasive biomarkers for progression of chronic kidney disease

Project description:To identify urinary RNA as non-invasive biomarkers for progression of chronic kidney disease

2018-10-31 | GSE121978 | GEO

Analysis of microRNA expression in ADPKD patient derived urinary exosomes by RNAseq

Project description:This experiment was designed to identify changes in microRNA expression in patients with early or late stage ADPKD vs healthy controls. microRNA was isolated from urinary exosomes before high throughput sequencing. Expression levels was analysed using STRAND NGS software.

2021-01-01 | E-MTAB-8109 | biostudies-arrayexpress

Proteomic profiling of ubiquitylated proteins in urinary exosomes

Project description:Exosomes, derived from multivesicular bodies (MVBs), contain proteins and genetic materials from their cell of origin and are secreted from various cells types, including kidney epithelial cells. In general, it is thought that protein cargo is ubiquitylated, but that ubiquitin is cleaved by specific deubiquitylases during the process of cargo incorporation into MVBs. Here, we provide direct evidence that in vivo, deubiquitylation is not essential. Ubiquitin was detected within human MVBs and urinary exosomes by electron microscopy. Protein mass spectrometry identified >6000 proteins in human urinary exosomes, 15% of which were ubiquitylated with various topologies (K63>K48> K11>K6>K29>K33>K27). Ubiquitylated proteins involved in transcriptional regulation or solute transport were significantly enriched. Non-biased analysis of over-represented motifs uncovered a significant preference for basic amino acids upstream of the ubiquitylation site. The current studies demonstrate that in human epithelial cells, deubiquitylation of protein cargo is not necessary for MVB formation and exosome secretion and highlight that urinary exosomes are an enriched source for studying ubiquitin modifications in physiological or disease states.

2016-02-22 | PXD002645 | Pride

Differential miRNA expression profiling of urinary exosomes from normo- and microalbuminuric type 1 diabetic patients

2014-02-14 | GSE48318 | GEO

Urinary phosphate-containing nanoparticle contributes to inflammation and kidney injury in salt-sensitive hypertension

Project description:Although disturbed phosphate metabolism frequently accompanies chronic kidney disease, it is unclear whether it contributes to the progression of renal dysfunction. Here, we show that urinary phosphate-containing nanoparticles promote kidney injury in salt-sensitive hypertension. Remarkably, four weeks of high salt loading resulted in a 2.5-fold increase in urinary phosphate excretion in Dahl salt-sensitive rats on a normal phosphorus diet. Inhibition of intestinal phosphate absorption using sucroferric oxyhydroxide (SF) in this model suppressed phosphaturia, attenuating glomerulosclerosis and tubulointerstitial injury without significantly affecting serum phosphate, blood pressure, or urinary sodium levels. In the kidney, macrophage infiltration and inflammatory cytokine induction were ameliorated by SF. Additionally, macrophage infiltration but not myofibril hypertrophy was alleviated in the heart. In vitro, phosphate loading to proximal tubule cells significantly increased inflammatory cytokine Ccl2, which was abolished by the removal of phosphate-containing nanoparticles but not by the knockdown of phosphate transporter Slc34a1. Finally, transcriptome analysis revealed a potential role of complement C1q in renal inflammation associated with disturbed phosphate metabolism. These data demonstrate that increased phosphaturia promotes inflammation and renal injury from an early stage of salt-sensitive hypertension, and suggest the need for interventions against subclinical phosphate accumulation to improve the prognosis of hypertensive kidney disease.

2020-08-22 | GSE143440 | GEO

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