Multipotent stromal cell therapy for cavernous nerve injury-induced erectile dysfunction

• Published in: Journal of sexual medicine Vol. 9; no. 2; p. 385
• Main Authors: Albersen, Maarten, Kendirci, Muammer, Van der Aa, Frank, Hellstrom, Wayne J G, Lue, Tom F, Spees, Jeffrey L
• Format: Journal Article
• Language: English
• Published: Netherlands 01.02.2012
• Subjects: Animals; Disease Models, Animal; Erectile Dysfunction - therapy; Humans; Male; Multipotent Stem Cells - transplantation; Penis - innervation; Peripheral Nerve Injuries - therapy; Postoperative Complications - therapy; Prostatectomy; Stromal Cells - transplantation
• ISSN: 1743-6109
• DOI: 10.1111/j.1743-6109.2011.02556.x

Erectile dysfunction (ED) following radical prostatectomy (RP) is a result of inadvertent damage to the cavernous nerves that run close to the prostate capsula. The mechanisms behind the development of post-RP ED are increasingly recognized and include cavernosal fibrosis and cavernosal smooth muscle apoptosis, resulting from cavernous nerve degeneration due to neuropraxia. In recent years, cell-based therapies have received increasing attention regarding their potential for recovery of erectile function following cavernous nerve injury (CNI). Multipotent stromal cells (MSCs) are an attractive cell source for this application based on their regenerative potential and their clinical applicability. To review available evidence on the efficacy and mechanisms of action of MSC application for the treatment of ED, with an emphasis on ED following CNI. A nonsystematic review was conducted on the available English literature between 1966 and 2011 on the search engines SciVerse-sciencedirect, SciVerse-scopus, Google Scholar, and PubMed. MSCs from both bone marrow and adipose tissue have shown beneficial effects in a variety of animal models for ED. While MSC application in chronic disease models such as diabetes, aging, and hyperlipidemia may result in cell engraftment and possibly MSC differentiation, this observation has not been made in the acute CNI rat model. In the latter setting, MSC effects seem to be established by cell recruitment toward the major pelvic ganglion and local paracrine interaction with the host neural tissue. While the type of model may influence the mechanisms of action of this MSC-based therapy, MSCs generally display efficacy in various animal models for ED. Before translation to the clinic is established, various hurdles need to be overcome.