A low testosterone level impairs erectile function by increasing endocan expression in rat penile corpus cavernosum

Area of Science:

• Urology
• Endocrinology
• Molecular Biology

Background:

• The precise mechanism linking low testosterone to erectile dysfunction (ED) remains undetermined.
• Endocan, a marker of endothelial function, has an unclear role in erectile function under low testosterone conditions.

Purpose of the Study:

• To investigate if low testosterone inhibits erectile function by altering endocan expression in rat penile corpus cavernosum endothelial cells.
• To elucidate the role of endocan in the AKT/eNOS/NO signaling pathway in the context of low testosterone and ED.

Main Methods:

• Male Sprague-Dawley rats underwent castration, testosterone treatment, or transfection with lentiviral vectors to manipulate endocan expression.
• Measurements included intracavernous pressure, mean arterial pressure, serum testosterone, nitric oxide (NO) levels, and expression of endocan, AKT, and eNOS.

Main Results:

• Castration significantly increased endocan expression and decreased erectile function (ICPmax/MAP), AKT/eNOS phosphorylation, and NO levels.
• Transfection to downregulate endocan in castrated rats reversed these effects, improving erectile function and restoring signaling pathway activity.

Conclusions:

• Increased endocan expression in low-testosterone states inhibits the AKT/eNOS/NO pathway, leading to ED in rats.
• Downregulating endocan in the penile corpus cavernosum presents a potential therapeutic strategy for hypoandrogenism-induced ED.