Neuropraxia Following Nerve Sparing Radical Prostatectomy Is Associated With Increased Expression Of Markers Of Inflammation And Fidgetin-2 Like Protein

Radical prostatectomy (RP) carries a high risk of erectile dysfunction (ED) as a result of neuropraxia. Neuropraxia also occurs when nerve sparing procedures are utilized. Preliminary data from our group has demonstrated that a previously uncharacterized microtubule severing enzyme that controls axonal growth in vitro, called Fidgetin-like 2 protein (FL2), is rapidly upregulated in the major pelvic ganglion (MPG) following cavernous nerve (CN) transection. Interestingly, animals that undergo surgical procedures without CN transection (SHAM), also had increased FL2 protein and mRNA expression. The objective of the present study was to test the hypothesis that even in the absence of direct damage to the CN, trauma associated with nerve sparing RP triggers an inflammatory and FL2 response which results in neuropraxia and thereby ED. ∼300g Sprague Dawley Rats were subjected to bilateral nerve transection surgery (CNI) or (SHAM). Animals were sacrificed at 6h, 2days and 3 days post-surgery and both MPG removed and total protein and RNA isolated. FL2 expression was assessed by western Blot and RT-qPCR. Immune factors were assayed by RT-qPCR.