MP47-12 TIME COURSE OF APOPTOTIC NEURONAL CELL DEATH IN THE MAJOR PELVIC GANGLION FOLLOWING CAVERNOUS NERVE INJURY

Abstract

You have accessJournal of UrologySexual Function/Dysfunction/Andrology: Basic Research II1 Apr 2014MP47-12 TIME COURSE OF APOPTOTIC NEURONAL CELL DEATH IN THE MAJOR PELVIC GANGLION FOLLOWING CAVERNOUS NERVE INJURY Johanna Hannan, Maarten Albersen, Joseph Watson, Xiaopu Liu, Petter Hedlund, Arthur Burnett, and Trinity Bivalacqua Johanna HannanJohanna Hannan More articles by this author , Maarten AlbersenMaarten Albersen More articles by this author , Joseph WatsonJoseph Watson More articles by this author , Xiaopu LiuXiaopu Liu More articles by this author , Petter HedlundPetter Hedlund More articles by this author , Arthur BurnettArthur Burnett More articles by this author , and Trinity BivalacquaTrinity Bivalacqua More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2014.02.1465AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail Introduction and Objectives Surgical treatments for prostate, bladder and colorectal cancers often lead to neuronal damage and erectile dysfunction (ED). Despite nerve-sparing techniques, ED prevails and preventing neurodegeneration is of great importance. This study aimed to characterize the markers of neuronal injury and apoptosis in the major pelvic ganglion (MPG) following bilateral cavernous nerve injury (BCNI). Methods Male Sprague-Dawley rats underwent sham or BCNI and MPGs were collected 2, 7, 14, 21, 30 and 60 days following BCNI (n=5/group). MPG gene expression analysis by qPCR was performed for markers of neuronal injury: activating transcription factor 3 (ATF3), glial fibrillary acidic protein (GFAP); apoptotic markers: caspase 1, caspase 3, caspase 9, Bcl2–associated X protein (Bax), BRCA1-associated RING domain protein 1 (BARD1); and neuronal markers: β-tubulin3 (BT3), tyrosine hydroxylase (TH), vesicular acetylcholine transporter (VAChT) and neuronal nitric oxide synthase (nNOS). Additional injured MPGs were fixed, embedded in paraffin and assessed for apoptosis by TUNEL (n=4/group). Results GFAP and ATF3 gene expression were significantly increased in MPGs from 2-21 days following BCNI (p<0.05). Apoptotic markers caspase1, caspase3, Bax and BARD1 at 2-14 days after BCNI were significantly elevated (p<0.05). There was no change in caspase 9 gene expression. Neuronal markers BT3, TH, and VACht were significantly lower in 2 and 7 day injured MPGs (p<0.05). Furthermore, 2 and 7 days following BCNI nNOS gene expression was 50% lower than sham (p<0.05). Apoptotic positive cells were significantly increased in MPGs 7 and 14 days following BCNI (Sham: 0.3±0.12, 7d: 9.5±1.2, 14d: 9.7±3.5, p<0.05). Conclusions Markers of neuronal injury and apoptosis are significantly increased early following BCNI. Further studies inhibiting the apoptotic pathway at these early time points may provide therapeutic avenues for neurogenic-mediated ED. © 2014FiguresReferencesRelatedDetails Volume 191Issue 4SApril 2014Page: e522-e523 Advertisement Copyright & Permissions© 2014MetricsAuthor Information Johanna Hannan More articles by this author Maarten Albersen More articles by this author Joseph Watson More articles by this author Xiaopu Liu More articles by this author Petter Hedlund More articles by this author Arthur Burnett More articles by this author Trinity Bivalacqua More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...