Analysis of microRNA expression in ADPKD patient derived urinary exosomes by RNAseq
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina HiSeq 2000
ORGANISM(S): Homo sapiens
SUBMITTER: Andrew Streets
PROVIDER: E-MTAB-8109 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Urinary exosomal miRNA profiling was conducted in urinary exosomes obtained from 8 healthy controls (C), 8 patients with type II diabetes (T2D) and 8 patients with type II diabetic nephropathy (DN) using Agilent´s miRNA microarrays.
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Project description:Analysis of microRNA expression in ADPKD patient derived urinary exosomes by RNAseq
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Project description:Autosomal dominant polycystic kidney disease (ADPKD) is a common cause of ESRD. Affected individuals inherit a defective copy of either the PKD1 or PKD2 gene, encoding the proteins polycystin?1 (PC1) or polycystin?2 (PC2) respectively. PC1 and PC2 are secreted on urinary exosome?like vesicles (ELVs) (100nm diameter vesicles), where PC1 is present in a cleaved form and may be complexed with PC2. Label free quantitative proteomic studies of urine ELVs in an initial discovery cohort (13 PKD1 and 18 Normals), revealed that of 2008 ELV proteins, nine (0.32%) showed a statistically significant difference between PKD1 and normals at a p<0.025. PC1 was reduced to 54% of the normal level (p<0.02) and PC2 reduced to 53% (p<0.001). TMEM2, a protein with homology to fibrocystin, the product of the polycystic hepatic and kidney disease (PKHD1) gene, is increased 2.1 fold (p<0.025). The PC1/TMEM2 ratio correlated inversely with height adjusted total kidney volume (HtTKV) in the discovery cohort and the ratio of PC1/TMEM2 or PC2/TMEM2 could be used to distinguish PKD1 from normals in a confirmation cohort. In summary, this study suggests that a test based on the urine exosomal PC1/TMEM2 or PC2/TMEM2 ratio may have utility in the diagnosis and perhaps monitoring of PKD1.
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Project description:To investigate the potential noninvasive early biomarkers of AD in 5XFAD mouse model, we investigate the proteome of urinary exosomes present in 1-month-old (before amyloid-β accumulation) 5XFAD mouse models and their littermate controls. Another two groups of 2 and 6 months-old urinary samples were collected for monitoring the dynamic change of target proteins during AD progression.
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Project description:Novel therapies in autosomal dominant polycystic kidney disease (ADPKD) signal the need for markers of disease progression or response to therapy. This study aimed to identify disease-associated proteins in urinary extracellular vesicles (uEVs), which include exosomes, in patients with ADPKD. We performed quantitative proteomics on uEVs using a labeled approach (healthy vs. ADPKD) and then using a label-free approach in different subjects (healthy vs. ADPKD vs. non-ADPKD chronic kidney disease [CKD]). In both experiments, thirty proteins were consistently more abundant (≥ 2-fold) in ADPKD-uEVs compared with healthy and CKD uEVs. Of these proteins, periplakin, envoplakin, villin-1, complement C3 and C9 were selected for confirmation, because (1) they were also significantly overrepresented in pathway analysis, and (2) they have been previously implicated in the pathogenesis of ADPKD. Immunoblotting was used to validate the proteomics results, confirming higher abundances of the selected proteins in ADPKD-uEVs in three independent groups of ADPKD-patients. While villin-1, periplakin and envoplakin were more abundant in advanced stages of the disease, complement was already higher in uEVs of young ADPKD patients with preserved renal function. Furthermore, all five proteins correlated positively with height adjusted total kidney volume. The proteins of interest were also analyzed in kidney tissues from kidney-specific-tamoxifen-inducible Pkd1-deletion mice, demonstrating higher expression in more severe stages of the disease. In summary, proteomic analysis of uEVs identified plakins and complement as disease-associated proteins in ADPKD. These proteins are new candidates for evaluation as biomarkers or targets for therapy in ADPKD.
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Project description:Changes in microRNA expression levels were identified by microarray. Samples were human kidney epithelial cell lines derived from patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) and unaffected controls. Autosomal Dominant Polycystic Kidney Disease (ADPKD), the most common inherited kidney disease, is due to mutations in PKD1 (85%) or PKD2 (15%) but has a highly variable phenotypic disease expression. We conducted parallel microarray profiling in normal and diseased human PKD1 cystic kidney cells to identify altered signatures of microRNA and mRNA target genes potentially implicated in disease expression. This dataset contains the results of the microRNA analysis.
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