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[Effects of castration on apoptosis and transforming growth factor-beta 1 mRNA in the neonatal mouse seminal
N Tanji1, S A Rahman, M Yokoyama
1Department of Urology, School of Medicine, Ehime University.
Background:
In the adult male rat prostate, castration induces apoptosis of epithelial cells concomitant with the increase in transforming growth factor-beta 1 (TGF-beta 1). In the present study, we investigated the effects of castration on apoptosis and TGF-beta 1 mRNA in neonatal mouse seminal vesicles.
Methods:
5-day-old BALB/c mice were castrated by Pfeifer's method. We estimated the weight, 3H-thymidine uptake by whole seminal vesicles, the amount of TGF-beta 1 mRNA by RT-PCR method, and the apoptotic index of both epithelium and mesenchyme.
Results:
The castration of 5-day-old neonatal mice resulted in much less weight of seminal vesicles and DNA synthesis estimated by 3H-thymidine uptake by whole seminal vesicles compared to intact neonatal mice, indicating that the growth of neonatal mouse seminal vesicles depends on androgens secreted by the testis. The amount of TGF-beta 1 mRNA estimated by RT-PCR method increased 4 days after castration at 5 days of age. However, the castration did not induce apoptosis in the seminal vesicles.
Conclusion:
The present study indicates that castration of neonatal mice does not induce apoptosis in the seminal vesicles, although it does a transient increase in TGF-beta 1 mRNA in the seminal vesicles.
Insights
Castration of neonatal mice reduces seminal vesicle growth and DNA synthesis. While transforming growth factor-beta 1 (TGF-beta 1) mRNA levels increase transiently, castration does not induce apoptosis in these vesicles.
Area of Science:
- Reproductive biology
- Developmental endocrinology
- Cellular and molecular biology
Context:
- Androgens are crucial for the development and maintenance of male reproductive organs.
- Previous studies in adult rats showed castration induces apoptosis in the prostate and increases TGF-beta 1.
- The role of androgens and TGF-beta 1 in neonatal seminal vesicle development was unclear.
Purpose:
- To investigate the effects of castration on seminal vesicle apoptosis and TGF-beta 1 mRNA expression in neonatal mice.
- To determine the role of androgens in the growth and DNA synthesis of neonatal seminal vesicles.
Summary:
- Castration of 5-day-old mice significantly reduced seminal vesicle weight and DNA synthesis, confirming androgen dependence.
- Transforming growth factor-beta 1 (TGF-beta 1) mRNA levels showed a transient increase 4 days post-castration.
- Contrary to findings in adult rats, castration did not induce apoptosis in the seminal vesicle epithelium or mesenchyme.
Impact:
- Demonstrates that neonatal mouse seminal vesicles are androgen-dependent for growth.
- Highlights a differential response to castration in neonatal seminal vesicles compared to adult prostates regarding apoptosis.
- Suggests TGF-beta 1 may play a role in seminal vesicle development independent of castration-induced apoptosis in neonates.