Mingxue Liu, Jing Liu, Xing Liu, Guanghui Wei
文献索引：J. Pediatr. Urol. 10(3) , 474-81, (2014)
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In previous studies, we established an animal model of human congenital hydronephrosis with exposure of developing mice to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), but the etiopathogenesis is not entirely clear. The present study was to identify the changes that may be involved in the etiology at the protein level.C57BL/6J mice fetuses were treated with TCDD. Comparative proteomic analysis was adopted to identify the proteins associated with hydronephrosis induced by TCDD.Two-dimensional electrophoresis display revealed that 19 protein spots were differentially expressed in the upper urinary tract tissues in fetal mice after exposure to TCDD. Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS) identified 12 up-regulated proteins: peroxiredoxin I (Prx I), cadherin 6, gamma-actin, radixin, desmin, type II transforming growth factor-beta receptor, chromogranin B, serum albumin precursor, transferrin, hypothetical protein LOC70984, lipk protein, and zinc finger protein 336. Histochemical staining indicated that Prx I protein was positively expressed in the ureteric epithelium in the treated group, and not in the control group, which is consistent with MALDI-TOF-MS.Prx I protein may be a potential biomarker or responsive protein of hydronephrosis in fetal mice induced by TCDD.Copyright © 2013 Journal of Pediatric Urology Company. Published by Elsevier Ltd. All rights reserved.
