Abstract

ObjectiveThe introduction of nerve-sparing radical prostatectomy represents a milestone in the treatment of prostate cancer. However, a certain percentage of cancer survivors still suffer from erectile dysfunction. Recent research has stated that using PDE 5-inhibitors after radical prostatectomy may lead to biochemical recurrence. This study was performed to identify the expression profile of small RNA in rats with neurogenic erectile dysfunction, and to investigate possible genes and signaling pathways involving in the disease.MethodsNeurogenic erectile dysfunction (ED) was induced in male rats by bilateral cavernous nerve crushing injury (BCNI). After 28 days, erectile function was evaluated by cavernous nerve electrostimulation. Masson’s trichrome staining was performed to assess histologic changes. RNA was isolated from the corpus cavernosum (CC) of both control rats and neurogenic ED rats. Small RNA sequencing was conducted using an Illumina Hiseq 2,500/2,000 platform. Candidate small RNAs were validated by real-time polymerase chain reaction.ResultsIntracavernous pressure (ICP) was significantly decreased in BCNI group compared with SHAM group. Corporal tissue in the neurogenic ED rats showed a significantly lower smooth muscle/collagen ratio compared with tissue in the SHAM controls. Real time PCR validated that miR-9a-5p, miR-203a-5p, miR-378a-3p and miR-3557-5p were upregulated, and meanwhile miR-3084a-3p was downregulated.ConclusionsSmall RNA, including microRNA, may play an important role in the regulation of genes in CC and some certain miRs may participate in post-prostatectomy ED. Further studies will be designed to investigate the specific mechanisms of these changes.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.