Abstract

Radical prostatectomy (RP), including nerve sparing RP (NSRP), carries high risk of erectile dysfunction (ED) through a mechanism primarily thought to involve neuropraxia of the cavernous nerve (CN). Activation of the inflammatory response has been proposed to contribute to neuropraxia. In preliminary studies, using a rat model of NSRP, we observed significant ED 3-days postsurgery accompanied by upregulation of inflammatory markers in the CN. We have also observed that using siRNA to downregulate an inhibitor of axonal growth called Fidgetin-like 2 protein (FL2) in a rat model of bilateral CN transection, promoted a more rapid regeneration of the CN and recovery of erectile function. Given the proposed association between inflammation, FL2 and CN repair, the objective of the present study was to determine if even in the absence of direct damage to the CN, trauma associated with NSRP triggers an inflammatory response or modulation of FL2 expression which contributes to neuropraxia and ED.

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