Decreased abundance of urinary exosomal aquaporin-1 in renal ischemia-reperfusion injury.

@article{Sonoda2009DecreasedAO,
  title={Decreased abundance of urinary exosomal aquaporin-1 in renal ischemia-reperfusion injury.},
  author={Hiroko Sonoda and Naoko Yokota-Ikeda and Sayaka Oshikawa and Yosuke Kanno and Kazuya Yoshinaga and Kazuyuki Uchida and Yuuji Ueda and Kouichi Kimiya and Shigehiro Uezono and Akira Ueda and Katsuaki Ito and Masahiro Ikeda},
  journal={American journal of physiology. Renal physiology},
  year={2009},
  volume={297 4},
  pages={
          F1006-16
        }
}
Urinary exosomes, secreted into urine from renal epithelial cells, are known to contain many types of renal functional membrane proteins. Here, we studied whether renal ischemia-reperfusion (I/R) affects urinary exosomal aquaporin-1 (AQP1) excretion in rats subjected to renal I/R and patients who underwent renal transplantation. Immunoblotting studies demonstrated reduction of the urinary exosomal AQP1 level even at 6 h after renal I/R, and the level continued to be low over 96 h after I/R… 

Figures and Tables from this paper

Characterization of urinary exosomal release of aquaporin-1 and -2 after renal ischemia-reperfusion in rats.

Results suggest that urinary exosomal release of AQP1 and AQP2 is reduced in I/R-induced AKI, whereas that of Alix and TSG101 is increased in the initial phase of renal fibrosis.

Urinary excretion pattern of exosomal aquaporin-2 in rats that received gentamicin.

Data from this study strongly suggest that the use of urinary exosomal AQP2 as a biomarker may allow detection of gentamicin-induced collecting duct cell dysfunction, and might also be useful for the early detection of GentamicIn-induced renal injury in addition to collecting duct injury.

Decreased Excretion of Urinary Exosomal Aquaporin-2 in a Puromycin Aminonucleoside-Induced Nephrotic Syndrome Model

Data suggest that UE-AQP2 is decreased in PAN-induced nephrotic syndrome and that this reflects its renal expression in the marked proteinuria phase after PAN treatment.

Excretion of urinary exosomal AQP2 in rats is regulated by vasopressin and urinary pH.

The data suggest that an increased plasma level of vasopressin promoted the excretion of urinary exosomal AQP2 and that urine alkalinization also increased it independently of vasipressin.

Acetazolamide enhances the release of urinary exosomal aquaporin-1.

The present findings indicate that AZ increases the release of exosomal AQP1 into urine in association with enhanced apical membrane expression of AQP 1.

Urinary extracellular vesicular release of aquaporins in patients with renal transplantation

Results indicate that acute diuresis after renal transplantation might be due to a decrease in the renal expression of AQP2, whose level can be estimated from the amount released in uEVs.

An Early Decrease in Release of Aquaporin-2 in Urinary Extracellular Vesicles After Cisplatin Treatment in Rats

The data suggest that uEV-AQP2 can be used to detect early renal impairment due to cisplatin, and a combination of u EVs and AQP1 may be useful for estimation of cis platin-induced renal injury in a stage-dependent manner.

mRNAs in urinary nano-extracellular vesicles as potential biomarkers for non-invasive kidney biopsy

Results suggest that changes in mRNA levels of urinary NVs reflect the disease status of kidney tissues and their functional alterations and may be used as a liquid biopsy tool for improved classification and performance of risk prediction to determine the severity of kidney diseases.

The effects of calcineurin inhibitors on epithelial electrolyte transport

Evidence is provided that CNIs influence a number of renal sodium transport proteins that may contribute towards the development of hypertension following transplantation, and an important role for calcineurin in the regulation of blood pressure and sodium transport in the kidney is suggested.
...

References

SHOWING 1-10 OF 30 REFERENCES

EPO and alpha-MSH prevent ischemia/reperfusion-induced down-regulation of AQPs and sodium transporters in rat kidney.

EPO and/or alpha-MSH treatment significantly prevent I/R-induced injuries such as urinary-concentrating defects and down-regulation of renal AQPs and sodium transporters.

Reduced abundance of aquaporins in rats with bilateral ischemia-induced acute renal failure: prevention by α-MSH.

The I/R injury is associated with markedly reduced expression of the collecting duct and proximal tubule AQPs, in association with an impairment of urinary concentration in the postischemic period.

Reduced abundance of aquaporins in rats with bilateral ischemia-induced acute renal failure: prevention by alpha-MSH.

The I/R injury is associated with markedly reduced expression of the collecting duct and proximal tubule AQPs, in association with an impairment of urinary concentration in the postischemic period.

Urinary excretion of aquaporin-2 in rat is mediated by a vasopressin-dependent apical pathway.

In Brattleboro rats or lithium-treated normal rats completely lacking vasopressin action, and hence having extremely low levels of AQP2 in the apical plasma membrane, AQP 2 was undetectable in urine, indicating that AQP1 is excreted predominantly via a selective apical pathway and not by whole cell shedding.

Exosomal Fetuin-A identified by proteomics: a novel urinary biomarker for detecting acute kidney injury.

Proteomic analysis of urinary exosomes can provide biomarker candidates for the diagnosis of AKI and urinary Fetuin-A might be a predictive biomarker of structural renal injury.

Collection, storage, preservation, and normalization of human urinary exosomes for biomarker discovery.

It is concluded that protease inhibitors are essential for preservation, and storage at -80 degrees C with extensive vortexing after thawing maximizes the recovery of urinary exosomes, suggesting minimal protein degradation in the urinary tract/bladder.

Aquaporin-1 facilitates epithelial cell migration in kidney proximal tubule.

Evidence is provided for the involvement of AQP1 in migration of proximaltubule cells and possibly in the response of the proximal tubule to injury in the intact kidney.

Large-scale proteomics and phosphoproteomics of urinary exosomes.

Overall, the analysis identified 1132 proteins unambiguously, including 177 that are represented on the Online Mendelian Inheritance in Man database of disease-related genes, suggesting that exosome analysis is a potential approach to discover urinary biomarkers.

Identification and proteomic profiling of exosomes in human urine.

The results indicate that exosome isolation may provide an efficient first step in biomarker discovery in urine and identify numerous protein components of MVBs and of the endosomal pathway in general.

Discovery of Urinary Biomarkers*

Most large scale biomarker discovery studies reported thus far have used one of two approaches to identify proteins and peptides whose excretion in urine changes in specific disease states: 1) two-dimensional electrophoresis with mass spectrometric and/or immunochemical identification of proteins and 2) top-down mass spectrumetric methods (SELDI-TOF-MS and capillary electrophore-MS).