MP31-14 CHANGES IN APOPTOSIS RELATED PROTEINS IN THE BLADDER AFTER PARTIAL BLADDER OUTLET OBSTRUCTION RELIEF

Abstract

You have accessJournal of UrologyBenign Prostatic Hyperplasia: Basic Research1 Apr 2015MP31-14 CHANGES IN APOPTOSIS RELATED PROTEINS IN THE BLADDER AFTER PARTIAL BLADDER OUTLET OBSTRUCTION RELIEF Ki Hak Song, Chong koo Sul, Yong gil Na, Jae sung Lim, Ju Hyun Shin, and Jong mok Park Ki Hak SongKi Hak Song More articles by this author , Chong koo SulChong koo Sul More articles by this author , Yong gil NaYong gil Na More articles by this author , Jae sung LimJae sung Lim More articles by this author , Ju Hyun ShinJu Hyun Shin More articles by this author , and Jong mok ParkJong mok Park More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2015.02.1369AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Partial bladder outlet obstruction (PBOO) induces prolonged bladder over-distension, leading to bladder dysfunction and structural alterations via induction of apoptosis. The aim of present study was to investigate sequential course of the apoptosis in bladder tissue, and changes of apoptosis related proteins in PBOO and subsequent relief. METHODS The study was conducted using 60 female Sprague-Dawley rats (body weight 250–300 g), divided into sham operated group (n=20), PBOO only (n=20), and PBOO group plus subsequent relief (n=20). PBOO rats were induced for 2 weeks, the obstruction has relived by removal of ligation after 2 weeks. After PBOO and relief surgery, urodynamic studies measuring contraction interval and contraction pressure were done. The tissues of rats were assessed by histologic anaylsis (H&E and TUNNEL stain) and expression of apoptosis related receptors (such as caspase-3, Erk, Jnk, P38, Bax, Bcl-2 and Survivin) have detected by RT-PCR and Western blotting. RESULTS Filling cystometry studies showed a significant decrease in contraction interval and increase in contraction pressure in the PBOO group. TUNNEL positive cells were significantly increased in PBOO group compared to sham operated group and decreased in PBOO relief group compared to PBOO group. On RT-PCR and Western blotting, expression of Bax, caspase-3, P38 and Jnk was significantly increased in PBOO group. But, expression of Erk, Bcl-2 was significantly decreased in PBOO group. The expression of Erk and Bcl-2 was significantly increased in PBOO relief group compared to PBOO group. CONCLUSIONS PBOO induced apoptosis of bladder tissue is associated with imbalance of MAPK pathways and apoptosis related protein. These results may also imply that pro-survival Erk kinase cascade is activated in response ischemic bladder injury and associated with initiation of bladder protection after PBOO. However, the mechanism of Survivin as anti-apoptotic factor in ischemic bladder tissue remains unclear. © 2015 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 193Issue 4SApril 2015Page: e361 Advertisement Copyright & Permissions© 2015 by American Urological Association Education and Research, Inc.MetricsAuthor Information Ki Hak Song More articles by this author Chong koo Sul More articles by this author Yong gil Na More articles by this author Jae sung Lim More articles by this author Ju Hyun Shin More articles by this author Jong mok Park More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...