Teng Hou1, Xiong Yang2, Bo Hai2, Bing Li2, Wencheng Li2, Feng Pan2, Min Chen2, Fuqing Zeng2, Xiaomin Han2. 1. Department of Urology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology Wuhan 430022, China ; State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine Guangzhou, GD 510060, China. 2. Department of Urology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology Wuhan 430022, China.
Abstract
AIM: To investigate the urothelial changes in the pathogenesis of ureteropelvic junction obstruction (UPJ-O). METHODS: A total of 12 patients of UPJ-O were respectively studied. The expression of Annexin A7, Annexin A11, EGFR, Keratin 5, uroplakin III, and SMA in the urothelium of obstructed UPJ segment and of the normal ureter below the obstructed segment were determined by immunofluorescence. Transmission electron microscopy was used to determine the morphological changes in UPJ epithelium in compared to normal ureteral epithelium. RESULTS: We found that Annexin A7, Annexin A11, EGFR, Keratin 5, and SMA were upregulated, while uroplakin III was downregulated in the urothelium of UPJ-O patients. Furthermore, ultrastructural analyses showed that intercellular spaces between urothelial cells were dilated and the number of microvilli on superficial cells was increased in UPJ-O patients. CONCLUSIONS: We propose that a disrupted urothelial barrier in UPJ-O may results in urothelial inflammatory response and truncated differentiated urothelial cells, which may play an important role in the development and pathogenesis of UPJO.
AIM: To investigate the urothelial changes in the pathogenesis of ureteropelvic junction obstruction (UPJ-O). METHODS: A total of 12 patients of UPJ-O were respectively studied. The expression of Annexin A7, Annexin A11, EGFR, Keratin 5, uroplakin III, and SMA in the urothelium of obstructed UPJ segment and of the normal ureter below the obstructed segment were determined by immunofluorescence. Transmission electron microscopy was used to determine the morphological changes in UPJ epithelium in compared to normal ureteral epithelium. RESULTS: We found that Annexin A7, Annexin A11, EGFR, Keratin 5, and SMA were upregulated, while uroplakin III was downregulated in the urothelium of UPJ-O patients. Furthermore, ultrastructural analyses showed that intercellular spaces between urothelial cells were dilated and the number of microvilli on superficial cells was increased in UPJ-O patients. CONCLUSIONS: We propose that a disrupted urothelial barrier in UPJ-O may results in urothelial inflammatory response and truncated differentiated urothelial cells, which may play an important role in the development and pathogenesis of UPJO.