Different Sex Steroidal Responses in Adult Mouse Prostate and in Fetal Urogenital Sinus.
- Author:
Sung Joon HONG
1
;
Byung Ha CHUNG
;
Dong Hyeon LEE
Author Information
1. Yonsei University Medical College, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
estrogen;
mouse
- MeSH:
Acinar Cells;
Adult*;
Animals;
Atrophy;
Castration;
Compensation and Redress;
Dihydrotestosterone;
Epithelium;
Estradiol;
Estrogens;
Gonadal Steroid Hormones;
Humans;
Hyperplasia;
Mice*;
Prostate*;
Prostatic Hyperplasia;
Rats
- From:Korean Journal of Urology
1997;38(4):335-350
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The currently proposed factors inducing prostatic hyperplasia are the combined effect of androgen and estrogen and the reawakening of the embryonic growth potential of mature prostatic stroma. This experiment was designed to find out any histological or structural differences occurring after compensating sex hormones on the mature prostate and the implanted fetal urogenital sinus (UGS) tissue which possesses a differentiating potential under the same condition. The ventral lobe of the rat prostate with implanted fetal UGS showed 4.4 fold increase in weight compared to the non-implanted contralateral ventral lobe. After the castration, both ventral lobes showed marked atrophy, and no further progress in differentiation occurred in the implanted UGS. Dihydrotestosterone (DHT) compensation after castration revealed a significant increase in weight in the mature prostate but the ventral lobe with the implanted UGS showed relatively low recovery rate in weight than in non-castrated control group. The compensation of estradiol after the castration showed little difference in mature prostate compared to castrated control group, but the UGS implanted ventral lobe revealed a relative stromal hyperplasia. Unlike the single-hormone compensation, the mature prostate displayed the characteristic hyperplasia of epithelium of each acinar lumen, but the UGS dearly showed the formation of new acini with nodular pattern when compensated with both DHT and estradiol. The level of DHT showed a significant correlation with the height of the prostatic acinar cell which differentiated from the UGS, and an inverse correlation with the stroma/epithelium ratio of implanted group. The serum concentration of estradiol showed a significant correlation with the relative volume of juxta-prostatic tissues, such as the coagulating gland and the adjacent stroma. From the above results, it might be assumed that the estrogen may have an important role in the embryonic stroma-mediated initiation of nodular hyperplastic changes of microacini under the influence of DHT and the determination of histologic pattern after initiation might be controlled by the prostatic DHT concentration.