In this work, we continue our ongoing efforts to determine what role neuropathy plays in ED development and to better understand the molecular mechanisms that regulate maintenance of penile architecture. We have shown that SHH inhibition causes apoptosis and that SHH protein is significantly decreased following CN injury. The localization of apoptosis in the corpora cavernosa after CN injury and after SHH inhibition appears very similar, with apoptotic cells present in the sinusoid smooth muscle and endothelium (Fig. 7). These results suggest that decreased SHH protein may be a cause of the abundant apoptosis that occurs following CN injury.
They also suggest that corpora cavernosa SHH signaling is regulated by neural innervation. When SHH protein was introduced into the corpora cavernosa at the time of CN injury, SHH was able to prevent apoptosis in a dose-dependent manner. These results show that SHH stabilizes the alterations of the corpora cavernosal smooth muscle following nerve injury. If penile apoptosis could be prevented while the cavernous nerve regenerates, the potential for preservation of erectile function would be substantial.