Urinary exosomal expression of activator of G protein signaling 3 in polycystic kidney disease.

Autor: Keri KC; Department of Medicine, Division of Nephrology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI, 53226, USA., Regner KR; Department of Medicine, Division of Nephrology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI, 53226, USA. kregner@mcw.edu., Dall AT; Department of Medicine, Division of Nephrology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI, 53226, USA., Park F; Department of Pharmaceutical Sciences, University of Tennessee Health Science Center College of Pharmacy, 881 Madison Ave, Rm 442, Memphis, TN, 38163, USA.
Jazyk: angličtina
Zdroj: BMC research notes [BMC Res Notes] 2018 Jun 07; Vol. 11 (1), pp. 359. Date of Electronic Publication: 2018 Jun 07.
DOI: 10.1186/s13104-018-3467-6
Abstrakt: Objective: PKD is a genetic disease that is characterized by abnormally proliferative epithelial cells in the kidney and liver. Urinary exosomes have been previously examined as a source of unique proteins that may be used to diagnose and monitor the progression of PKD. Previous studies by our group have shown that AGS3, which is a receptor-independent regulator G-proteins, was markedly upregulated in RTECs during kidney injury including PKD. In this study, our goal was to determine whether AGS3 could be measured in exosomes using animals and humans with PKD.
Results: In our study, urinary exosomes were isolated from PCK rats and the control Sprague-Dawley (SD) rats. AGS3 expression was significantly increased (P < 0.05) in PKD versus SD rats at 16 weeks of age. This increase was detectable in a time-dependent manner from 8 weeks of age and peaked at ~ 16-20 weeks (length of study). Similarly, in exosomes from human urine samples with PKD, AGS3 expression was significantly increased (P < 0.05) compared to healthy human controls where AGS3 was largely undetectable. In conclusion, the detection of AGS3 in urinary exosomes may be a novel biomarker for PKD, and provide new insight into the biology of tubular epithelial cell function during cystic disease progression.
Databáze: MEDLINE
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