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BioMed Research International
Volume 2017 (2017), Article ID 9531074, 8 pages
https://doi.org/10.1155/2017/9531074
Research Article

Cytoplasmic Localization of WT1 and Decrease of miRNA-16-1 in Nephrotic Syndrome

1Departamento de Microbiología e Inmunología, Facultad de Ciencias Biológicas, Universidad Autónoma de Nuevo León (UANL), 66450 San Nicolás de los Garza, NL, Mexico
2Laboratorios de Inmunología y Biología Molecular, Unidad Académica de Ciencias Biológicas, Universidad Autónoma de Zacatecas (UAZ), 98040 Zacatecas, ZAC, Mexico
3Hospital General Zacatecas “Luz González Cosío”, Ciudad Gobierno, 98160 Zacatecas, ZAC, Mexico

Correspondence should be addressed to Pablo Zapata-Benavides

Received 11 September 2016; Revised 9 January 2017; Accepted 23 January 2017; Published 19 February 2017

Academic Editor: Jae I. Shin

Copyright © 2017 Pablo Zapata-Benavides et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Nephrotic syndrome (NS) is a glomerular disease that is defined by the leakage of protein into the urine and is associated with hypoalbuminemia, hyperlipidemia, and edema. Steroid-resistant NS (SRNS) patients do not respond to treatment with corticosteroids and show decreased Wilms tumor 1 (WT1) expression in podocytes. Downregulation of WT1 has been shown to be affected by certain microRNAs (miRNAs). Twenty-one patients with idiopathic NS (68.75% were SSNS and 31.25% SRNS) and 10 healthy controls were enrolled in the study. Podocyte number and WT1 location were determined by immunofluorescence, and the serum levels of miR-15a, miR-16-1, and miR-193a were quantified by RT-qPCR. Low expression and delocalization of WT1 protein from the nucleus to the cytoplasm were found in kidney biopsies of patients with SRNS and both nuclear and cytoplasmic localization were found in steroid-sensitive NS (SSNS) patients. In sera from NS patients, low expression levels of miR-15a and miR-16-1 were found compared with healthy controls, but only the miR-16-1 expression levels showed statistically significant decrease (). The miR-193a expression levels only slightly increased in NS patients. We concluded that low expression and delocalization from the WT1 protein in NS patients contribute to loss of podocytes while modulation from WT1 protein is not associated with the miRNAs analyzed in sera from the patients.