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Protein expression in vesicoureteral reflux: What about children?

膀胱输尿管反流 发病机制 医学 胶质细胞源性神经生长因子 免疫印迹 回流 泌尿科 污渍 基因 内科学 病理 生物 受体 遗传学 疾病 神经营养因子
作者
Eda Tokat,Mustafa Tan,Serhat Gürocak
出处
期刊:Journal of Pediatric Surgery [Elsevier BV]
卷期号:57 (3): 492-496 被引量:1
标识
DOI:10.1016/j.jpedsurg.2021.04.017
摘要

Pathogenesis of vesicoureteral reflux (VUR) which concerns improper embryonal ureteric bud development still remains controversial, despite current studies have revealed several candidate genes. In this study, we aimed to determine the protein expression of certain genes which might play role in the pathogenesis of VUR, in the resected ureterovesical junction segments.The study group consisted of 19 children; 12(63%) girls, 7(37%) boys who had ureteroneocystostomy (UNC) operation; 3(15.7%) right sided, 7(36.8%) left sided, 9(47.3%) bilateral due to VUR. As a total, 28 ureterovesical junction segments were available for analysis of protein expressions of GDNF/RET, PAX2 and FGFR2 genes by their Western Blot analysis.Protein based expressions of FGFR2, PAX2 and RET were significantly lower than β-Actin (p = 0.001, for all proteins). Correlation analyses between grade of reflux and protein expressions revealed no significant relations (p>0.05, for all proteins). When we grouped the patients into 2 groups as high grade (grade 4-5) and low grade reflux (grade 1-3) for convenient analyses, no statistically significant difference was found between groups (p>0.05, for all proteins). Renal units were also grouped according to differential functions (≥40% and <40%) obtained by renal scintigraphy and compared in terms of proteins' expressions. There was also no significant difference between two groups regarding FGFR2, PAX2 and RET band areas (p>0.05, for all proteins).Our study revealed decreased protein expressions of GDNF/RET, PAX2 and FGFR2 genes in the patients with VUR. Relation between clinical parameters and expression levels were statistically uncorrelated. Prospective studies of larger sample size are necessary in order to delineate the impact of certain proteins in the etiopathogenesis of VUR.
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