The male accessory sex organs and epididymis regress following androgen depletion, although the onset of apoptosis varies temporally depending upon the tissue type. Transforming growth factor-beta1 (TGF-beta1) is an androgen-repressed gene and believed to be an apoptotic agent in the regressing rat ventral prostate (VP). Hence, in order to investigate the status of TGF-beta isoforms following castration in androgen-dependent tissues other than VP, this study was undertaken. Northern blot analysis using total RNA from these tissues of intact animals showed higher levels of TGF-beta1 expression as compared with VP, indicating a function other than that of an apoptotic agent for this isoform. Following orchiectomy, TGF-beta1 was induced in all organs studied and the levels were highest at day 3 following castration in seminal vesicle (SV) and the epididymis and decreased by day 5 despite the absence of androgens. This observation implies that TGF-beta1 might not be a truly androgen-repressed gene in these tissues. TGF-beta2 was up-regulated in VP, SV, caput and corpus epididymis but was undetectable in the dorsolateral prostate and cauda epididymis. On the other hand, TGF-beta3 expression was refractory to the androgen status in corpus epididymis and SV but was up-regulated in the remaining tissues. The castration-induced induction of mRNAs was attenuated after exogenous androgen administration. Most importantly, all the isoforms differed significantly in the time and magnitude of induction following castration, suggesting that a single hormone, testosterone, modulates the expression of TGF-betas in an isoform- and tissue-specific manner.

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