Relevant bibliographies by topics / Urinary exosome

Academic literature on the topic 'Urinary exosome'

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Published: 11 March 2023

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Journal articles on the topic "Urinary exosome"

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Huang, Kun, Sudha Garimella, Alyssa Clay-Gilmour, Lucia Vojtech, Bridget Armstrong, Madison Bessonny, and Alexis Stamatikos. "Comparison of Human Urinary Exosomes Isolated via Ultracentrifugation Alone versus Ultracentrifugation Followed by SEC Column-Purification." Journal of Personalized Medicine 12, no. 3 (February 24, 2022): 340. http://dx.doi.org/10.3390/jpm12030340.

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Chronic kidney disease is a progressive, incurable condition that involves a gradual loss of kidney function. While there are no non-invasive biomarkers available to determine whether individuals are susceptible to developing chronic kidney disease, small RNAs within urinary exosomes have recently emerged as a potential candidate to use for assessing renal function. Ultracentrifugation is the gold standard for urinary exosome isolation. However, extravesicular small RNA contamination can occur when isolating exosomes from biological fluids using ultracentrifugation, which may lead to misidentifying the presence of certain small RNA species in human urinary exosomes. Therefore, we characterized human urinary exosomal preparations isolated by ultracentrifugation alone, or via ultracentrifugation followed by size exclusion chromatography (SEC) column-purification. Using nanoparticle tracking analysis, we identified SEC fractions containing robust amounts of exosome-sized particles, that we further characterized using immunoblotting. When compared to exosomal preparations isolated by ultracentrifugation only, SEC fractionated exosomal preparations showed higher levels of the exosome-positive marker CD81. Moreover, while the exosome-negative marker calnexin was undetectable in SEC fractionated exosomal preparations, we did observe calnexin detection in the exosomal preparations isolated by ultracentrifugation alone, which implies contamination in these preparations. Lastly, we imaged SEC fractionated exosomal preparations using transmission electron microscopy to confirm these preparations contained human urinary exosomes. Our results indicate that combining ultracentrifugation and SEC column-purification exosome isolation strategies is a powerful approach for collecting contaminant-free human urinary exosomes and should be considered when exosomes devoid of contamination are needed for downstream applications.
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Abdeen, Ahmed, Hiroko Sonoda, Ragab El-Shawarby, Saki Takahashi, and Masahiro Ikeda. "Urinary excretion pattern of exosomal aquaporin-2 in rats that received gentamicin." American Journal of Physiology-Renal Physiology 307, no. 11 (December 1, 2014): F1227—F1237. http://dx.doi.org/10.1152/ajprenal.00140.2014.

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Urinary exosomes are nano-sized vesicles secreted into urine from all types of renal epithelial cells and are known to contain possible biomarker proteins for renal diseases. Gentamicin has been reported to decrease the level of renal aquaporin (AQP)2, which is known to be mainly expressed in renal collecting ducts and excreted into the urine via exosomes. In the present study, we investigated whether urinary exosomal AQP2 could serve as a potential biomarker for gentamicin-induced nephrotoxicity, especially collecting duct cell dysfunction. Gentamicin was given to rats intraperitoneally once every day starting on day 0. Gentamicin significantly increased the plasma creatinine concentration from day 5 and beyond. Also, gentamicin induced polyuria and a defective urine concentration mechanism on day 7, suggesting gentamicin-induced collecting duct cell dysfunction. Immunoblot analysis showed that gentamicin significantly increased urinary exosomal AQP2 excretion on day 1 but decreased it on day 7 compared with the control group. Similarly, increased excretion of exosomal tumor susceptibility gene 101 protein, frequently used as an exosome marker protein, was observed on day 1. However, gentamicin did not significantly affect the urinary excretion of exosomal tumor susceptibility gene 101 on day 7. Gentamicin slightly decreased renal AQP2 expression on day 2 and markedly decreased it on day 8. These data strongly suggest that the use of urinary exosomal AQP2 as a biomarker may allow detection of gentamicin-induced collecting duct cell dysfunction. Furthermore, urinary exosomal AQP2 might also be useful for the early detection of gentamicin-induced renal injury in addition to collecting duct injury.
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Liu, Yu-Ru, and Yi-Fen Lee. "Urinary exosome and beyond." Translational Cancer Research 5, S2 (August 2016): S321—S324. http://dx.doi.org/10.21037/tcr.2016.07.16.

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Xiang, Xiaochao, Fulin Guan, Fenglong Jiao, Hang Li, Wanjun Zhang, Yangjun Zhang, and Weijie Qin. "A new urinary exosome enrichment method by a combination of ultrafiltration and TiO2 nanoparticles." Analytical Methods 13, no. 13 (2021): 1591–600. http://dx.doi.org/10.1039/d1ay00102g.

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The workflow of separation and enrichment of exosomes by ultrafiltration–TiO2. We proposed a new strategy for facile exosome isolation from human urine by utilizing the ultrafiltration technique and TiO2, which can significantly reduce urine volumes, increase exposure of the material to exosomes in urine and obtain high purity exosomes.
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Lv, Lin-Li, Yu-Han Cao, Hai-Feng Ni, Min Xu, Dan Liu, Hong Liu, Ping-Sheng Chen, and Bi-Cheng Liu. "MicroRNA-29c in urinary exosome/microvesicle as a biomarker of renal fibrosis." American Journal of Physiology-Renal Physiology 305, no. 8 (October 15, 2013): F1220—F1227. http://dx.doi.org/10.1152/ajprenal.00148.2013.

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Micro (mi)RNAs are frequently dysregulated in the development of renal fibrosis. Exosomes are small membrane vesicles that could be isolated from urine secreted from all nephron segments. Here we sought to observe for the first time whether miRNA in urine exosome could serve as a potential biomarker of renal fibrosis. Urine samples were collected from 32 chronic kidney disease (CKD) patients who underwent kidney biopsy and 7 controls. Exosome was isolated and confirmed by immunogold staining of exosome marker. Members of miR-29, miR-200, and RNU6B as endogenous control were detected by RT quantitative PCR. Electronic microscopy verified a typical shape of exosome with average size of 65.1 nm and labeled it with anti-CD9 and anti-aquaporin 2 antibody. Members of miR-29 and miR-200 are readily measured with reduced levels compared with controls ( P < 0.05) and can robustly distinguish CKD from controls [area under the curve (AUC) varied from 0.902 to 1 by receiver operating characteristics analysis]. miR-29c correlated with both estimated glomerular filtration rate ( r = 0.362; P < 0.05) and degree of tubulointerstitial fibrosis ( r = −0.359; P < 0.05) for CKD patients. Moreover, miRNA in exosome was decreased in mild fibrosis group compared with moderated to severe group. miR-29a and miR-29c could predict degree of tubulointerstitial fibrosis with AUC of 0.883 and 0.738 ( P < 0.05). The sensitivity and specificity for distinguishing mild from moderate to severe fibrosis were 93.8 and 81.3% with the use of miR-29a and 68.8 and 81.3% for miR-29c. Overall, miR-29c in urinary exosome correlates with both renal function and degree of histological fibrosis, suggesting it as a novel, noninvasive marker for renal fibrosis.
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Garcia-Vives, Eloi, Cristina Solé, Teresa Moliné, Marta Vidal, Irene Agraz, Josep Ordi-Ros, and Josefina Cortés-Hernández. "The Urinary Exosomal miRNA Expression Profile is Predictive of Clinical Response in Lupus Nephritis." International Journal of Molecular Sciences 21, no. 4 (February 18, 2020): 1372. http://dx.doi.org/10.3390/ijms21041372.

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Data on exosomal-derived urinary miRNAs have identified several miRNAs associated with disease activity and fibrosis formation, but studies on prognosis are lacking. We conducted a qPCR array screening on urinary exosomes from 14 patients with biopsy-proven proliferative lupus glomerulonephritis with a renal outcome of clinical response (n = 7) and non-response (n = 7) following therapy. Validation studies were performed by qRT-PCR in a new lupus nephritis (LN) cohort (responders = 22 and non-responders = 21). Responder patients expressed significantly increased levels of miR-31, miR-107, and miR-135b-5p in urine and renal tissue compared to non-responders. MiR-135b exhibited the best predictive value to discriminate responder patients (area under the curve = 0.783). In vitro studies showed exosome-derived miR-31, miR-107, and miR-135b-5p expression to be mainly produced by tubular renal cells stimulated with inflammatory cytokines (e.g IL1, TNFα, IFNα and IL6). Uptake of urinary exosomes from responders by mesangial cells was superior compared to that from non-responders (90% vs. 50%, p < 0.0001). HIF1A was identified as a potential common target, and low protein levels were found in non-responder renal biopsies. HIF1A inhibition reduced mesangial proliferation and IL-8, CCL2, CCL3, and CXCL1 mesangial cell production and IL-6/VCAM-1 in endothelial cells. Urinary exosomal miR-135b-5p, miR-107, and miR-31 are promising novel markers for clinical outcomes, regulating LN renal recovery by HIF1A inhibition.
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Ledet, Elisa M., Patrick J. Miller, Ratish Gambhira, Aryeneesh Dotiwala, and A. Oliver Sartor. "Characterization of plasma-derived and urinary exosomal microRNA from metastatic CRPC patients." Journal of Clinical Oncology 34, no. 2_suppl (January 10, 2016): 248. http://dx.doi.org/10.1200/jco.2016.34.2_suppl.248.

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248 Background: Exosomes are nano-sized (50-100nm) vesicles derived from normal and tumor cells that function in cell-cell communication. These vesicles and their nucleic acid cargo may potentially serve as biomarkers for assessment of risk stratification and therapeutic response. The goal of this study was to characterize exosome derived microRNA (miRNA) isolated from plasma (pExos) and urine (uExos) of metastatic CRPC patients. Methods: Plasma samples were obtained from 18 mCRPC patients and 1 normal control. Following exosome isolation, RNA extraction and library prep, paired-end sequencing was performed using Illumina Hi-Seq 2000. A bioinformatics pipeline was used for data processing including alignment, duplicate removal, normalization, and variant calling. Visualization and differential analyses were performed with SNP & Variation Suite v8.x. RNA derived from uExos was amplified using whole transcriptome amplification and interrogated with Prostate Cancer (PCa) miScript miRNA PCR Array. Results: Exosomes from both plasma and urine had similar amounts of miRNA/total RNA with average 34% miRNA (range 19%-51%). pExos had larger RNA fragments (range 10-333 nt) while uExos were more highly fragmented (range 10-60 nt). The amount of miRNA and fragmentation pattern was highly variable amongst patients. In pExos, RNA from PDPK1, USP9X, MAGI2, HMGA2 and PTGFR were present and previously shown in PCa. Also in pExos, miR941-2, miR4454, miR1302-2, miR143HG and miR22HG were annotated in prostate cancer patients; these miRNA have previously been identified in cancer. In uExos miR-16-5p and miR-375 were present and are shown to be differentially regulated in prostate cancer. Expression analyses will be presented. PCR validation is ongoing. Conclusions: The identification of cancer associated miRNA in pExos and uExos may potentially serve as biomarkers in mCRPC patients. The abundance and stability of miRNA contained in exosomes may provide insight into tumor evolution and disease progression. Additional studies evaluating the clinical relevance and prognostic value of exosomal miRNA are warranted.
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Shirley, James Forrest, Joshua Drourr, W. Taylor Edwards, Kubra Tuna, Lisa K. Ryan, Abdel Alli, Ying Tang, and Sarah C. Glover. "Mast Cells in Patients with Hereditary α-Tryptasemia Promote HLA-DR Expression and a Th2-Polarizing Microenvironment in the Gastrointestinal Tract." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 192.13. http://dx.doi.org/10.4049/jimmunol.202.supp.192.13.

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Abstract Hereditary α-tryptasemia (HαT) is a recently identified, genetic disorder characterized by multisystem comorbidities resulting from increased monoallelic α-tryptase copy number (CN) at TPSAB1 (α-TPSAB1). Affected individuals frequently exhibit heterogeneous multisystem symptoms and comorbidities which negatively impact daily functioning and quality of life. In the cohorts examined thus far, functional dyspepsia and irritable bowel syndrome, were most frequently reported. However, the mechanism by which increased α-TPSAB1 CN produces GI disease is unknown. Tryptase is almost exclusively produced by mast cells (MC). In the gut, MC play important roles in immune responses, leukocyte recruitment, neuroimmune inflammation, and tissue repair. MC can also promote T-cell activation and polarization via cytokine secretion, co-stimulatory marker expression and MHC II antigen presentation. MCs also release exosomes, nanosized vesicles secreted by most cell types present in biological fluids such as blood, cerebrospinal fluid, and urine, which have a reported influence on T cell differentiation. In early experiments, we found increased numbers of GI MCs, activated T cells, and urinary exosomes in HαT patients compared to healthy donors. Thus, we evaluated MC surface antigen expression, exosome proteomics, and cytokine expression of exosome-treated T cells. We found increased HLA-DR and FcɛR1α expression in HαT-patient GI MCs, increased Th2 associated signaling proteins in HαT urinary exosomes, and elevated Th2 cytokine expression in HαT-exosome treated T cells. These results suggest that HαT GI morbidity involves aggravated MC hyperplasia and antigen presentation which promotes T cell activation and Th2 polarization.
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El Fekih, Rania, James Hurley, Vasisht Tadigotla, Areej Alghamdi, Anand Srivastava, Christine Coticchia, John Choi, et al. "Discovery and Validation of a Urinary Exosome mRNA Signature for the Diagnosis of Human Kidney Transplant Rejection." Journal of the American Society of Nephrology 32, no. 4 (March 3, 2021): 994–1004. http://dx.doi.org/10.1681/asn.2020060850.

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BackgroundDeveloping a noninvasive clinical test to accurately diagnose kidney allograft rejection is critical to improve allograft outcomes. Urinary exosomes, tiny vesicles released into the urine that carry parent cells’ proteins and nucleic acids, reflect the biologic function of the parent cells within the kidney, including immune cells. Their stability in urine makes them a potentially powerful tool for liquid biopsy and a noninvasive diagnostic biomarker for kidney-transplant rejection.MethodsUsing 192 of 220 urine samples with matched biopsy samples from 175 patients who underwent a clinically indicated kidney-transplant biopsy, we isolated urinary exosomal mRNAs and developed rejection signatures on the basis of differential gene expression. We used crossvalidation to assess the performance of the signatures on multiple data subsets.ResultsAn exosomal mRNA signature discriminated between biopsy samples from patients with all-cause rejection and those with no rejection, yielding an area under the curve (AUC) of 0.93 (95% CI, 0.87 to 0.98), which is significantly better than the current standard of care (increase in eGFR AUC of 0.57; 95% CI, 0.49 to 0.65). The exosome-based signature’s negative predictive value was 93.3% and its positive predictive value was 86.2%. Using the same approach, we identified an additional gene signature that discriminated patients with T cell–mediated rejection from those with antibody-mediated rejection (with an AUC of 0.87; 95% CI, 0.76 to 0.97). This signature’s negative predictive value was 90.6% and its positive predictive value was 77.8%.ConclusionsOur findings show that mRNA signatures derived from urinary exosomes represent a powerful and noninvasive tool to screen for kidney allograft rejection. This finding has the potential to assist clinicians in therapeutic decision making.
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Cao, Yuhan, Yuanhui Shi, Yuwei Wang, Yanlang Yang, Wenjun Guo, Cuifeng Zhang, Wenjun Pei, and Cong Fu. "Exosomal hsa_circ_0008925 from Urine Is Related to Chronic Renal Fibrosis." Disease Markers 2022 (February 18, 2022): 1–10. http://dx.doi.org/10.1155/2022/1899282.

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At present, there is no noninvasive biomarker of renal fibrosis. The potential diagnostic value of urinary exosome-derived circRNAs from glomerular disease patients for renal fibrosis is still uncertain. Here, we first detected the expression of hsa_circ_0008925 in TGF-β1-cultured HK-2 cell-derived exosomes. Secondly, we collected urine samples from 95 biopsy-proven glomerular disease patients and 34 healthy controls. The expression of hsa_circ_0008925 was analyzed, and the correlation with renal function and pathological changes was calculated. The receiver operating characteristic (ROC) curve for the diagnosis of renal fibrosis was performed. The results showed that in exosomes derived from TGF-β1-cultured HK-2 cells, the expression of hsa_circ_0008925 was increased compared with normal cultured. Further, the expression level of hsa_circ_0008925 was increased in urinary exosomes from renal fibrosis patients and correlated with serum creatinine, blood urea nitrogen (BUN), estimated glomerular filtration rate, and cystatin C. The level of hsa_circ_0008925 was furthermore correlated with the score of tubulointerstitial fibrosis (TIF) and the score of glomerular sclerosis. The ROC curve showed that hsa_circ_0008925 can diagnose renal fibrosis at a cut-off value of 0.093 with a sensitivity of 52.2% and specificity of 96.4%. In summary, we indicated that urinary exosomal hsa_circ_0008925 could be acted as a noninvasive biomarker for renal fibrosis in glomerular diseases patients.
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Dissertations / Theses on the topic "Urinary exosome"

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Hiemstra, Thomas Francois. "Investigating the biology of urinary exosomes." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610116.

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Burballa, Tàrrega Carla 1988. "Discovery of putative prognostic and therapeutic miRNA in uEVs of Dent's Disease 1 patients and characterisation of cellular models of the disease." Doctoral thesis, TDX (Tesis Doctorals en Xarxa), 2021. http://hdl.handle.net/10803/671807.

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Dent disease 1 (DD1) is a rare renal tubulopathy caused by CLCN5 mutations and characterized by low molecular weight proteinuria, variable hypercalciuria, nephrocalcinosis and/or nephrolithiasis and progression to kidney failure. The underlying mechanisms linking ClC-5 loss-of-function and endocytosis impairment in the renal proximal tubule (and other DD1 phenotypes) remain unknown. In this thesis we have followed three approaches to identify altered pathways by ClC-5 mutations: (1) conduct a European survey to analyse the prevalence and DD1 clinical features, (2) study miRNA expression profiles from DD1 patients’ urinary exosome-like vesicles (uEVs) to get insight into DD1 pathophysiological mechanisms and (3) characterisation of a DD1 cell model. The European survey showed that DD1 has a variable presentation. Our study of uEVs miRNA identified new pathophysiological pathways, which may lead to identify putative diagnostic and prognostic biomarkers. Finally, our cell model with different mutations provides a valuable prototype for additional investigation of impaired pathways.
La malaltia de Dent 1 (DD1) és una tubulopatia renal rara causada per mutacions en el gen CLCN5 i caracteritzada per proteinuria de baix pes molecular, hipercalciuria, nefrocalcinosi i/o litiasis renals així com progrés a insuficiència renal. Els mecanismes que causen la pèrdua de funció de ClC-5 i el defecte en l’endocitosi en el túbul proximal (entre d’altres fenotips de DD1) no es coneixen. En aquesta Tesi hem desenvolupat tres aproximacions per identificar vies alterades per mutacions en ClC-5. (1) hem fet una enquesta europea per analitzar la prevalença i les característiques clíniques de DD1, (2) hem estudiat l’expressió de miRNA en vesícules exosome-like urinàries (uEVs) per entendre els mecanismes fisiopatològics de la malaltia i (3) hem caracteritzat un model cel·lular de DD1. L’enquesta europea mostrà que DD1 té una presentació variable. El nostre estudi de miRNA en uEVs va permetre identificar nous mecanismes fisiopatològics que poden ser potencials biomarcadors diagnòstics i pronòstics de DD1. Finalment, el nostre model cel·lular amb diferents mutacions provà representar un prototip vàlid per investigacions addicionals del mecanismes desregulats.
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CORBETTA, SAMUELE. "Proteomica degli exosomi urinari per la ricerca di biomarcatori nella nefropatia diabetica e nelle tubulopatie ereditarie." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/76004.

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Le urine costituiscono il fluido biologico di elezione nella ricerca di biomarcatori per le patologie renali in quanto possono essere raccolte in modo semplice e non invasivo; una strategia per la semplificazione del proteoma urinario è rappresentata dall’isolamento degli exosomi urinari (UE), nanovescicole di membrana (30-100 nm) rilasciate dalle cellule epiteliali nello spazio urinario. In questo lavoro abbiamo focalizzato l’attenzione sulla nefropatia diabetica (DN), una comune complicazione del diabete ed una delle cause più frequenti di insufficienza renale terminale (ESDR), e sulle tubulopatie ereditarie (SLTs), un gruppo eterogeneo di malattie genetiche rare dell’età pediatrica caratterizzate da difetti in proteine coinvolte nel riassorbimento di sodio-cloruro a livello dell’ansa di Henle e/o dei tubuli renali distali, come i cotrasportatori NCC NKCC2, alterati rispettivamente nella sindrome di Gitelman (GS) e nella sindrome di Bartter1 (B1). L’obiettivo che ci siamo proposti è stato quello di studiare il proteoma degli UE in: 1) un modello animale di DN, i ratti ZDF (Zucker Diabetic Fatty), e corrispondenti controlli, per l’identificazione di potenziali biomarcatori diagnostici/prognostici e 2) pazienti affetti da SLTs e controlli sani al fine di proporre un approccio diagnostico complementare/alternativo all’analisi genetica e fornire un punto di partenza per la ricerca di biomarcatori. Per quanto riguarda lo studio della DN, sono state raccolte le urine delle 24 ore da 7 ratti ZDF e controlli a differenti età per monitorare l’evoluzione della DN, gli UE sono stati isolati mediante ultracentrifugazione, seguita da caratterizzazione biochimica. Dopo l’allestimento di un pool rappresentativo di UE di ratti ZDF e controlli a 20 settimane, ne è stato analizzato il proteoma tramite LC-ESI-MS/MS portando all’identificazione ed alla quantificazione label-free di 286 proteine. Il contenuto differenziale di alcune di queste proteine è stato confermato tramite immunoblotting; il contenuto della Major-Urinary-Protein-1 è risultato significativamente più alto, quello della proteina Xaa-Pro-Dipeptidase più basso e quello della Neprilisina invariato, rispettivamente, negli UE di ratti ZDF rispetto ai controlli. Per quanto riguarda le SLTs, la casistica era formata da 32 pazienti SLTs già studiati dal punto di vista genetico e biochimico-clinico, da 4 pazienti SLTs non classificabili e da 22 controlli sani. Dopo la raccolta delle seconde urine del mattino, sono stati isolati e caratterizzati gli UE. I risultati hanno mostrato che il segnale relativo al cotrasportatore NCC risulta significativamente ridotto o assente negli UE dei pazienti GS rispetto ai controlli, e allo stesso modo il cotrasportatore NKCC2 per i pazienti B1. Le differenze nei livelli di queste due proteine negli UE ci consentono il riconoscimento dei pazienti GS e B1 rispetto ai controlli e, in combinazione con i dati biochimico-clinici, rispetto agli altri pazienti Bartter. E’ stato quindi proposto e validato statisticamente un approccio diagnostico che può risultare utile in casi di SLTs a diagnosi incerta. Per quanto riguarda la proteina NCC è stata inoltre effettuata una correlazione tra la quantità del trasportatore presente negli UE e la gravità della mutazione corrispondente. Per l’identificazione di biomarcatori delle altre due forme di SLTs studiate, la sindrome di Bartter2 (B2) e di Bartter3 (B3), abbiamo allestito un pool di UE, abbiamo separato le proteine mediante elettroforesi bidimensionale selezionando alcuni spot differenziali da analizzare tramite LC-ESI-MS/MS; il contenuto differenziale negli UE di alcune proteine identificate verrà validato mediante IB. In conclusione possiamo affermare che la composizione proteica degli UE risulta alterata in maniera riproducibile in presenza di nefropatia diabetica e di tubulopatie ereditarie; le differenze evidenziate possono costituire un punto di partenza per l’identificazione di biomarcatori diagnostici/prognostici e per il chiarimento dei meccanismi patogenetici di tali malattie.
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Miao, Yuxuan. "Mechanisms of Bacterial Expulsion as a Cell Autonomous Defense Strategy In the Bladder Epithelium." Diss., 2015. http://hdl.handle.net/10161/9862.

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Due to its close proximity to the gastrointestinal tract, the human urinary tract is

subjected to constant barrage by gut-­associated bacteria. However, for the most part, this tract has resisted infection by various microbes. The impregnability of the urinary tract to microbial colonization is attributable to the ability of the bladder to promptly sense and mount robust responses to microbial challenge. A powerful mechanism for the elimination of invading bacteria was recently described in bladder epithelial cells, involving non-­lytic ejection of intracellular bacteria back into the extracellular milieu. In spite of the effectiveness of this defense strategy, much of the underlying mechanisms surrounding how this powerful cellular defense activity detects intracellular UPEC and shuttles them from their intracellular location to the plasma membrane of BECs to be exported remains largely a mystery.

Here, we describe uropathogenic E.coli (UPEC) expelled from infected bladder

epithelium cells (BECs) within membrane-­bound vesicles as a distinct cellular defense

response. Examination of the intracellular UPEC revealed that intracellular bacteria were

initially processed via autophagy, the conventional degradative pathway, then delivered

into multivesicular bodies (MVBs) and encapsulated in nascent intraluminal vesicle membrane. We further show the bacterial expulsion is triggered when intracellular UPEC follow the natural degradative trafficking pathway and reach lysosomes and attempt to neutralize its pH to avoid degradation. This pathogen-­mediated activity is detected by mucolipin TRP channel 3 (TRPML3), a transient receptor potential cation channel localized on lysosomes, which spontaneously initiates lysosome exocytosis resulting in expulsion of exosome-­encased bacteria. These studies reveal a cellular default system for lysosome homeostasis and also, how it is coopted by the autonomous defense program to clear recalcitrant pathogens.


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Lai, Yue Fan, and 賴岳汎. "Searching Potential Protein Biomarkers of Bladder Cancer from Urinary Exosomes." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/58768233351293356294.

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碩士
長庚大學
生物醫學研究所
99
Bladder cancer mortality increases annually in Taiwan. The main detection tool for bladder cancer is cystoscopy. However, this method is an invasive and costly procedure. Urine is stored in bladder for hours and can be collected non-invasively. Therefore, urine can be a good material for discovery of bladder cancer biomarkers. Multivesicular body derived exosomes present in saliva, plasma, and urine. Previous studies pointed out that exosomes correlate with diseases, and can be a material for biomarker searching. In this work, we compared the proteomic profiles of urinary exosomes between controls and bladder cancer patients using isotopic dimethyl labelling and two-dimensional LC/MS/MS. The differentially-expressed exosomal proteins will be potential non-invasive biomarkers for detection of bladder cancer. Exosomes extracted from 9 hernia and 9 bladder cancer patients were pooled as a control and a bladder cancer samples, respectively. After digestion of exosomal proteins, peptides of hernia and bladder cancer samples were labelled with light and heavy dimethylation reagents, respectively. The labelled peptides were analyzed by on-line SCX/RP LC/MS/MS. The quantification of proteins were performed by MaxQuant software. We further used the dimethylation platform to compare the exosome proteins expressions of 9 hernia and 9 bladder cancer individuals without pooling samples. We have indentified total 3873 exosomal proteins in two comparisons, and 107 proteins show higher different concentration levels between bladder cancer and hernia patients. 29 of 107 proteins in urinary exosomes could directly quantified by multiple-reaction-monitoring (MRM)-MS. MRM-MS validated 29 proteins expression levels between 5 hernia and 5 bladder cancer patients’ exosomes, and most results were consistent with that we have seen in discovery phase. Then we validated more clinical sample. We quantified 29 proteins expression levels in 12 hernia, 28 bladder cancer, 5 hematuria and 3 urinary tract infection patients’ exosomes. 22 of 29 proteins had significant differentially expressed level between hernia and bladder cancer patient, and higher expressed level of 3 proteins in bladder cancer patients were not due to hematuria or urinary tract infection. In this work, we implemented two comparisons to searching differentially-expressed exosomal proteins, and we validated these proteins by MRM-MS. The validation results are consistent with prediction. In the future, we will increase the sample number to raise the reliability of these potential bladder cancer biomarkers.
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Lin, Shih-Yi, and 林詩怡. "Investigate the proteomics of urinary exosomes for biomarkers of urothelial carcinoma." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/59sj6j.

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博士
中國醫藥大學
臨床醫學研究所博士班
105
Purpose: Studies have focused on establishing noninvasive, rapid methods for discovering urothelial carcinoma (UC) biomarkers. The urinary exosome proteome is believed to directly reflect the proteome of UC, providing a suitable investigation resource. Increasingly applied matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) spectrometry facilitates reliable clinical diagnosis of bacteria. MALDI-TOF spectrometry, a rapid analytical platform, has not been used for urinary exosome analysis. Therefore, we used it for determining UC biomarkers. Experimental Design: From 2012 to 2015, we enrolled 129 consecutive patients with UC and 62 participants without UC. Exosomes from their urine were isolated, and the protein extracts of these exosomes were analyzed through MALDI-TOF spectrometry. Moreover, immunohistochemical (IHC) analysis of another 122 UC and 26 non-UC tissues was conducted to verify the discovered biomarkers. Results: Two peaks at m/z 5593 (fragmented peptide of alpha-1-antitrypsin; sensitivity, 50.4%; specificity, 96.9%) and m/z 5947 (fragmented peptide of histone H2B1K sensitivity, 62.0%; specificity, 92.3%) were identified as UC diagnosis exosome biomarkers. UC patients with detectable histone H2B1K showed 2.29- and 3.11-fold increased risks of recurrence and progression, respectively, compared with those with nondetectable histone H2B1K. Verification results of IHC staining revealed significantly higher expression of alpha 1-antitrypsin (p = 0.038) and H2B1K (p = 0.005) in UC tissues than in normal tissues. The expression of alpha 1-antitrypsin and H2B1K in UC tissues was significantly correlated with UC grades (p < 0.05). Conclusion: Urinary exosome proteins alpha 1-antitrypsin and histone H2B1K, which are identified through MALDI-TOF analysis, could facilitate rapid diagnosis and prognosis of UC.
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Book chapters on the topic "Urinary exosome"

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Salvi, Samanta, Erika Bandini, and Francesco Fabbri. "Urinary Exosomes in Prostate Cancer." In Urinary Biomarkers, 115–20. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1354-2_10.

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Alvarez-Llamas, Gloria, and Irene Zubiri. "Proteome of Human Urinary Exosomes in Diabetic Nephropathy." In Biomarkers in Kidney Disease, 347–67. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-7699-9_22.

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Alvarez-Llamas, Gloria, and Irene Zubiri. "Proteome of Human Urinary Exosomes in Diabetic Nephropathy." In Biomarkers in Kidney Disease, 1–21. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7743-9_22-1.

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Abdeen, Ahmed, Hiroko Sonoda, Ayae Tanaka, and Masahiro Ikeda. "Urinary Exosomes as a Possible Source of Kidney Disease Biomarkers." In Role of Exosomes in Biological Communication Systems, 221–44. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-6599-1_10.

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Pitto, Marina, Samuele Corbetta, and Francesca Raimondo. "Preparation of Urinary Exosomes: Methodological Issues for Clinical Proteomics." In Methods in Molecular Biology, 43–53. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1872-0_3.

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Barigazzi, Elisa, Lucia Santorelli, W. Morello, F. Raimondo, B. Crapella, L. Ghio, C. Tamburello, G. Montini, and M. Pitto. "New Insight into Idiopathic Nephrotic Syndrome: Strategy Based on Urinary Exosomes." In Toxic Chemical and Biological Agents, 217–18. Dordrecht: Springer Netherlands, 2020. http://dx.doi.org/10.1007/978-94-024-2041-8_13.

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Santorelli, Lucia, Elisa Barigazzi, M. Pitto, and F. Raimondo. "Investigation of the N-Glycoproteome in the Urinary Exosomes: Technical Challenges." In Toxic Chemical and Biological Agents, 257–58. Dordrecht: Springer Netherlands, 2020. http://dx.doi.org/10.1007/978-94-024-2041-8_26.

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Conde-Vancells, Javier, and Juan M. Falcon-Perez. "Isolation of Urinary Exosomes from Animal Models to Unravel Noninvasive Disease Biomarkers." In Liver Proteomics, 321–40. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-959-4_21.

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DiStefano, Johanna K., Rupesh Kanchi Ravi, and Mahdieh Khosroheidari. "Urinary Exosomes as Potential Source for Identification of Biomarkers for Kidney Damage: Comparing Methodologies." In Biomarkers in Disease: Methods, Discoveries and Applications, 939–54. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7696-8_47.

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Alvarez, M. Lucrecia. "Isolation of Urinary Exosomes for RNA Biomarker Discovery Using a Simple, Fast, and Highly Scalable Method." In RNA Mapping, 145–70. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1062-5_13.

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Conference papers on the topic "Urinary exosome"

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Blondal, Thorarinn, Anne I. Rasmussen, Anni R. Thomsen, Michael Borre, Jacob Fredsøe, Ditte Andreasen, Torben Falck Ørntoft, Karina D. Sørensen, and Peter Mouritzen. "Abstract 1943: A microRNA signature in urinary exosomes for diagnosis of prostate cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1943.

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Mouritzen, Peter, Jacob Christian Fredsøe, Thorarinn Blondal, Anne Karin Rasmussen, Michael Borre, Christa Haldrup, Ditte Andreasen, Niels Tolstrup, Torben Falck Ørntoft, and Karina Dalsgaard Sørensen. "Abstract B40: A two-microRNA signature in urinary exosomes for diagnosis of prostate cancer." In Abstracts: AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines; December 4-7, 2015; Boston, MA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.nonrna15-b40.

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Berner, K., M. Hirschfeld, G. Rücker, D. Weiß, A. Ritter, M. Jäger, I. Juhasz-Böss, and T. Erbes. "Urinary exosomal microRNAs as potential non-invasive biomarkers in breast cancer detection." In 40. Jahrestagung der Deutschen Gesellschaft für Senologie e.V. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1710603.

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Berner, K., M. Hirschfeld, G. Rücker, D. Weiß, A. Ritter, I. Juhasz-Böss, and T. Erbes. "Urinary exosomal microRNAs as potential non-invasive biomarkers in breast cancer detection." In Kongressabstracts zur Tagung 2020 der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe (DGGG). © 2020. Thieme. All rights reserved., 2020. http://dx.doi.org/10.1055/s-0040-1717838.

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Baumgart, Sophie, Joana Heinzelmann, Michael Stoeckle, Marie Stampe Ostenfeld, and Kerstin Junker. "Abstract 5182: Characterization of miRNA expression pattern fromin-vitroobtained exosomes of different urinary bladder cancer cell lines." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5182.

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Wilson, Brittany, Rebekah Betar, Alexander Martin, Zackaria Niazi, Michael Boyer, Lori Winter, Victor Babich, Francesca Di Sole, and Elitsa Ananieva. "Abstract 2377: microRNA expression profile in urinary exosomes is dependent on non-invasive lymphoma induction in mice." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2377.

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Berrondo, Claudia, Jonathan Flax, Aisha Siebert, Victor Kucherov, Alex Rosenberg, Christopher Fucile, and Carla Beckham. "Abstract B31: Bladder cancer patient urinary exosomes and tumors contain long noncoding RNA that may serve as therapeutic targets and biomarkers." In Abstracts: AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines; December 4-7, 2015; Boston, MA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.nonrna15-b31.

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Solé-Marcé, Cristina, Eloi Garcia-Vives, Irene Agraz, Josep Ordi-Ros, and Josefina Cortés-Hernández. "THU0236 URINARY EXOSOMAL MIR-31, MIR-107 AND MIR-135B-5P FROM TUBULAR RENAL CELLS AS RESPONDER BIOMARKER IN LUPUS NEPHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5346.

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