Wang Y, Puri P, Hassan J, Miyakita H, Reen D J
Children's Research Centre, Our Lady's Hospital for Sick Children, Dublin, Ireland.
J Urol. 1995 Aug;154(2 Pt 2):679-83. doi: 10.1097/00005392-199508000-00091.
The pathophysiology of ureteropelvic junction obstruction is unknown. Using specific antibodies, we studied specimens from 35 cases of ureteropelvic junction obstruction and 32 of normal ureteropelvic junction by immunohistochemistry using protein gene product 9.5 (a general neuronal marker), S100 (a supporting cell marker), synaptophysin (a neuromuscular junction marker) and nerve growth factor receptor. Nerve growth factor expression was examined at the messenger ribonucleic acid (mRNA) level using reverse transcription-polymerase chain reaction technique in 11 ureteropelvic junction obstruction specimens and 7 controls. The most striking finding was the marked reduction of protein gene product 9.5, synaptophysin and nerve growth factor receptor staining positive nerve fibers in the muscle layers of ureteropelvic junction obstruction compared to the normal ureteropelvic junction. Supporting nerve cell fibers (S100) were preserved in cases of ureteropelvic junction obstruction and normal ureteropelvic junction. A significantly less intense signal for nerve growth factor mRNA was found in the ureteropelvic junction obstruction specimens compared to normal ureteropelvic junction. These findings suggest that defective innervation may have an important role in the pathogenesis of ureteropelvic junction obstruction, and decreased nerve growth factor mRNA expression may be important in the etiology of ureteropelvic junction obstruction.
肾盂输尿管连接处梗阻的病理生理学尚不清楚。我们使用特异性抗体，通过免疫组织化学方法，用蛋白质基因产物9.5（一种通用的神经元标志物）、S100（一种支持细胞标志物）、突触素（一种神经肌肉接头标志物）和神经生长因子受体，研究了35例肾盂输尿管连接处梗阻病例和32例正常肾盂输尿管连接处的标本。使用逆转录-聚合酶链反应技术，在11例肾盂输尿管连接处梗阻标本和7例对照中，检测了信使核糖核酸（mRNA）水平的神经生长因子表达。最显著的发现是，与正常肾盂输尿管连接处相比，肾盂输尿管连接处梗阻肌层中蛋白质基因产物9.5、突触素和神经生长因子受体染色阳性神经纤维明显减少。在肾盂输尿管连接处梗阻病例和正常肾盂输尿管连接处中，支持神经细胞纤维（S100）得以保留。与正常肾盂输尿管连接处相比，在肾盂输尿管连接处梗阻标本中发现神经生长因子mRNA信号强度明显较低。这些发现表明，神经支配缺陷可能在肾盂输尿管连接处梗阻的发病机制中起重要作用，神经生长因子mRNA表达降低可能在肾盂输尿管连接处梗阻的病因中起重要作用。
