Reconstuctive UrologyReversing Urethral Hypovascularity Through Testosterone and Estrogen Supplementation
Section snippets
Animals
This study was fully approved by the Institutional Animal Care and Use Committee of Northwestern University (Protocol #IS00004702). Six non-castrate and 18 castrate male Sprague-Dawley rats (7 weeks old, weight 175-225g) were acquired from Charles River Laboratories (Wilmington, MA). The rats were surgically castrated at 6.5 weeks to ensure that they had achieved sexual maturity prior to castration. The rats were divided into 4 groups: noncastrate (NC) control, castrate non-supplemented (C),
Periurethral Vascularity (CD31 Expression)
Detailed expression results for CD31, AR, TIE-2, ER-alpha, and GPER1 expression are listed in Table 1 and photographs of immunohistochemistry staining patterns are displayed in Figure 1. In order to quantify vessel density, we evaluated expression of the endothelial cell marker CD31. Castrated rats demonstrated the lowest levels of CD31 expression and vessel density (3.62%, Fig. 2A), reinforcing that testosterone deprivation is associated with decreased periurethral vascularity. CD31 expression
COMMENT
Because many AUS cuff erosions occur in hypogonadal men, we wondered whether hormonal supplementation with testosterone or estrogen might reverse atrophic changes seen from hypogonadism in a rat urethra model. As proof of concept, we confirmed that the rat urethra demonstrates significantly lower angiogenesis in the absence of androgen compared to the urethras of noncastrate control animals, analogous to the human urethra.3 TRT restored periurethral vascularity comparable to that of noncastrate
CONCLUSION
We found that testosterone supplementation as well as estrogen supplementation restored periurethral vascularity in castrated (hypogonadal) rats. Both hormone therapies were associated with equivalent, if not superior, periurethral vascularity compared to noncastrate control animals. These results provide a basis for employing testosterone or estrogen in order to reverse the effects of hypogonadism in men at risk for AUS complications due to urethral atrophy.
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Financial Disclosure: The authors declare that they have no relevant financial interests.
Histology services were provided by the Northwestern University Histology and Phenotyping Core Laboratory which is supported by NCI P30-CA060553 awarded to the Robert H Lurie Comprehensive Cancer Center.