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• W2108264911 abstract "You have accessJournal of UrologyBladder Cancer: Basic Research I1 Apr 2015MP36-09 SCHISTOSOMA HAEMATOBIUM EGG-INDUCED BLADDER UROTHELIAL ABNORMALITIES ARE MODULATED BY P53 IN A GENDER-DEPENDENT FASHION Jared Honeycutt, Olfat Hammam, and Michael Hsieh Jared HoneycuttJared Honeycutt More articles by this author , Olfat HammamOlfat Hammam More articles by this author , and Michael HsiehMichael Hsieh More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2015.02.737AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES The bladder urothelium develops dynamic changes during Schistosoma haematobium infection (urogenital schistosomiasis). These alterations include hyperplasia, ulceration, dysplasia, squamous metaplasia and frank carcinogenesis. Defining the pathways underpinning these urothelial responses will contribute to a deeper understanding of how S. haematobium egg-induced expulsion, hematuria, and bladder cancer develop in humans. The tumor suppressor gene p53 is of particular interest, given its role in many cancers, including bladder cancer generally and schistosomal bladder cancer specifically. METHODS Transgenic mice featuring tamoxifen-inducible cre recombinase activity in cells expressing uroplakin-3a, a urothelial-specific gene (Upk3a-GCE mice) were crossed with either TdTomato-floxed-EGFP reporter or p53-floxed mice. Mice were administered tamoxifen or vehicle control to induce excision of floxed genes. TdTomato-EGFP reporter mice were sacrificed and their bladders harvested, sectioned, and imaged by fluorescence microscopy. P53-floxed mice underwent bladder wall injection with S. haematobium eggs or vehicle controls. Three months later, mice were sacrificed and their bladders subjected to histological analysis (H&E staining). RESULTS We first confirmed the phenotypic fidelity of Upk3a-GCE mice by crossing them with TdTomato-floxed-EGFP reporter mice and administering tamoxifen to their progeny. As expected, these progeny switched from TdTomato to EGFP expression in their bladder urothelium. Having confirmed the phenotype of Upk3a-GCE mice, we next crossed them to p53-floxed mice. The resulting progeny were given tamoxifen or vehicle control to render them urothelial p53-haploinsufficient or –intact, respectively. Then, we injected S. haematobium eggs or control vehicle into the bladder walls of these mice. Male p53-intact, egg-injected mice exhibited similar histological changes as their p53- haploinsufficient counterparts, including urothelial hyperplasia and ulceration. In contrast, female p53-intact, egg-injected mice featured no urothelial ulceration, whereas their p53-haploinsufficient counterparts often had significant ulceration. CONCLUSIONS Urothelial p53 signaling indeed seems to affect urothelial homeostasis during S. haematobium infection, albeit in a gender-specific manner. Ongoing work seeks to determine whether p53 mediates alterations in urothelial cell cycle status and frank carcinogenesis in the setting of urogenital schistosomiasis. © 2015 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 193Issue 4SApril 2015Page: e432 Advertisement Copyright & Permissions© 2015 by American Urological Association Education and Research, Inc.MetricsAuthor Information Jared Honeycutt More articles by this author Olfat Hammam More articles by this author Michael Hsieh More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ..." @default.
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• W2108264911 title "MP36-09 SCHISTOSOMA HAEMATOBIUM EGG-INDUCED BLADDER UROTHELIAL ABNORMALITIES ARE MODULATED BY P53 IN A GENDER-DEPENDENT FASHION" @default.
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