Since the renal epidermoid cyst is too rare, the mechanisms of squamous morphogenesis have not well characterized. A 73-year-old female was referred with an incidentally detected renal pelvis mass. Abdominopelvic computed tomography scan revealed a noncalcified soft tissue mass in the renal pelvis. Total nephroureterectomy was performed under the impression of a renal pelvis malignancy. The patient was discharged without postoperative complication. The outer surface of mass lesion was lined with urothelia and squamous epithelia, containing keratinous materials. The urothelia were positively stained against uroplakin II and cytokeratin 7, whereas almost of the squamous epithelia were negative with uroplakin II. The two different epithelia were generally sharply demarcated. Interestingly, some part of squamous epithelia contained uroplakin-positive and many more cytokeratin 7-positive cells. The atypical clinical features in our case can reconsider the diagnostic clues of renal epidermoid cysts that have been reported before, and the unique immunohistochemical results may understand the histogenetic implications of the lesion.
Epidermal Cyst ; Female ; Humans ; Keratin-7 ; Keratins ; Kidney ; Kidney Pelvis ; Morphogenesis ; Postoperative Complications ; Uroplakin II ; Uroplakins

The apical surface of mammalian urinary epithelium is covered by numerous scallop-shaped membrane plaques. This plaque consists of four different uroplakins (UPs) and integral membrane proteins. UPs, which are a member of the tetraspanin superfamily, are assembled into plaques that act as an exceptional barrier to water and toxic materials in urine. Within the plaques, the four UPs are organized into two heterodimers consisting of UP Ia/UP II and UP Ib/UP III in the endoplasmic reticulum. The two heterodimers bind to a heterotetramer, and then assemble into 16-nm particles in the Golgi apparatus. The aggregated UP complex ultimately covers almost all the mature fusiform vesicles in cytoplasm. These organelles migrate towards the apical urothelial cells, where they can fuse with the apical plasma membrane. As a result, the UPs are synthesized in large quantities only by terminally differentiated urothelial cells. For this reason, the UPs can be regarded as a major urothelial differentiation marker. In UP knockout (KO) mice, the incorporation of fully assembled UP plaques in cytoplasm into the apical surface is not functional. The mice with UP III-deficient urothelium show a significantly reduced number of UPs, whereas those with UP II-deficient urothelium have nearly undetectable levels of UPs. This finding strongly suggests that UP II ablation completely abolishes plaque formation. In addition, UP II KO mice contain abnormal epithelial polyps or complete epithelial occlusion in their ureters. UP IIIa KO mice are also associated with impairment of the urothelial permeability barrier and development of vesicoureteral reflux as well as a decrease in urothelial plaque size. In this review, I summarize recently published studies about UPs and attempt to explain the clinical significance of our laboratory results.
Animals ; Cell Membrane ; Cytoplasm ; Endoplasmic Reticulum ; Epithelium ; Golgi Apparatus ; Membrane Proteins ; Membranes ; Mice ; Models, Animal ; Organelles ; Permeability ; Polyps ; Ureter ; Urinary Tract ; Uroplakins ; Urothelium ; Vesico-Ureteral Reflux ; Water

PURPOSE: Prostatitis is a common condition with a significant effect on quality of life. Even though the etiology of chronic prostatitis remains unclear, certain bacterial infections may play a major role. In recent studies, E. coli, one important etiology of urinary tract infection, was found to mediate invasion into the bladder epithelium after binding uroplakin Ia in the apical membrane of the urinary bladder. Because E. coli is also an important pathogen for bacterial prostatitis, we investigated the uroplakin mRNA expression in micro-dissected mouse prostates. MATERIALS AND METHODS: We harvested the urinary bladder, ventral prostate, dorso-lateral prostate, and coagulating gland from 3 male imprinting control region (ICR) mice. The total RNA was extracted, cDNA was prepared, and finally the five target genes--uroplakin Ia, Ib, II, III, and beta-actin were amplified. We also examined the expressed sequence tags (EST) about above four uroplakin genes from mouse EST data. RESULTS: Uroplakin Ia, Ib, II, and III were expressed in the urinary bladder. However, only uroplakin Ia was definitively expressed in the ventral prostate. Uroplakin Ib and II were weakly expressed in the ventral, dorso-lateral, and coagulating prostate. Uroplakin III was not expressed in the prostate tissue. The mouse RNA transcripts in the EST data also showed similar results to uroplakin expression in the prostate. CONCLUSIONS: These results suggest that the mouse ventral prostate may be an adequate locus for acute or chronic bacterial prostatitis study. Further in-vitro bacteriologic studies of the ventral prostate will help reveal the mechanisms of chronic bacterial prostatitis.
Actins ; Animals ; Bacterial Infections ; DNA, Complementary ; Epithelium ; Expressed Sequence Tags ; Humans ; Male ; Membranes ; Mice ; Prostate ; Prostatitis ; Quality of Life ; RNA ; RNA, Messenger ; Urinary Bladder ; Urinary Tract Infections ; Uroplakin Ia ; Uroplakin Ib ; Uroplakin III ; Uroplakins

Interstitial cystitis/bladder pain syndrome (IC/BPS) is a heterogeneous syndrome which is usually characterized by urinary frequency, nocturia, and bladder pain. Several pathomechanisms have been proposed, including uroepithelial dysfunction, mast cell activation, neurogenic inflammation, autoimmunity, and occult urinary tract infections. It is possible that an inflammatory process alters regulation of urothelial homeostasis and results in dysfunction of the bladder epithelium. Different phenotypes of IC/BPS have been explored including Hunner and non-Hunner type IC, hypersensitive bladder, and bladder pain both with and without functional somatic syndrome. Different gene expressions have also been found in different IC phenotypes. Abnormal expressions of uroplakin, chondroitin sulfate and adhesive protein E-cadherin, tight junction protein zonula occludens-1 in IC/BPS bladder suggest abnormal epithelial differentiation in this bladder disease. Analysis of inflammatory proteins, or cytokines in the urine or serum provides another diagnostic foundation forIC/BPS subtypes. The involvement of IC/BPS in systemic functional somatic syndrome and other pelvic organ diseases might also subdivide subtypes of IC/BPS. Chronic inflammation, increased urothelial apoptosis, and abnormal urothelial function are closely associated in IC bladders. This article reviews recent research on the pathomechanisms of IC, which might help us in mapping the heterogeneity of the disease.
Adhesives ; Apoptosis ; Autoimmunity ; Biomarkers ; Cadherins ; Chondroitin Sulfates ; Cystitis ; Cytokines ; Epithelium ; Gene Expression ; Homeostasis ; Inflammation ; Lower Urinary Tract Symptoms ; Mast Cells ; Neurogenic Inflammation ; Nocturia ; Phenotype ; Population Characteristics* ; Tight Junctions ; Urinary Bladder ; Urinary Bladder Diseases ; Urinary Tract Infections ; Uroplakins

PURPOSE: The goal of this study was to constructing a nonviral vector, expressing the chimeric gene of the SV40 T antigen and mouse uroplakin II promoter (UPII promotor), which was uniquely expressed in the urothelium, to aid in the treatment of bladder cancer by the creation of a tumor that will express itself in the bladder only, but that will have no effect on the other urothelium. MATERIALS AND METHODS: 36 female C3H/He mice, weighing 20-25grams, were used in this study. A UPII-GFP-liposome complex was installed into the bladder, with Enhanced Green Fluorescent Protein (EGFP), expressing the bladder mucosa, and analyzed via fluorescent microscopy. A UPII- SV40T-liposome complex was then administered into the bladders of the mice, and the bladder and ureter examined, grossly and microscopically, at 1, 2, 3 and 4 weeks, to find transitional cell carcinomas specific to the bladder, the degree of bladder cancer development, and whether the development was from superficial to deep tumors, as well as tumor metastasis. RESULTS: The expression of EGFP was found in all four mice after 2 days. No development of tumors was evident in any mice. However, of the 6 mice sacrificed 28 days after bladder instillation, urothelial dysplasia was evident in 4. There was no evidence of transient cell carcinomas in the ureter or renal pelvis in any of the mice, or of distant metastasis during the term of the study. CONCLUSIONS: This model of bladder cancer seems to take longer than other models for cancer formation as the carcinogen affects the DNA of urothelial cell for the formation of bladder cancer. However, our bladder cancer model was better than others due to its similarity for the processes of normal bladder cancer formation.
Administration, Intravesical ; Animals ; Antigens, Viral, Tumor* ; Carcinoma, Transitional Cell ; DNA ; Female ; Humans ; Kidney Pelvis ; Liposomes ; Mice ; Microscopy ; Models, Theoretical* ; Mucous Membrane ; Neoplasm Metastasis ; Ureter ; Urinary Bladder Neoplasms* ; Urinary Bladder* ; Uroplakin II* ; Uroplakins* ; Urothelium