Desai, KV and Kondaiah, P (2000) Androgen ablation results in differential regulation of transforming growth factor-$\beta$ isoforms in rat male accessory sex organs and epididymis. In: Journal of Molecular Endocrinology, 24 (2). pp. 253-260.
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The male accessory sex organs and epididymis regress following androgen depletion although the onset of apoptosis varies temporally depending upon the tissue type. $TGF- \beta 1$ 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 $TGF- \beta 1$ expression as compared with VP, indicating a function other than that of an apoptotic agent for this isoform. Following orchiectomy, $TGF-\beta 1$ 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 implied that $TGF-\beta 1$ might not be truly androgen-repressed gene in these tissues. $TGF-\beta 2$ was upregulated in VP, SV, caput and corpus epididymis but was undetectable in the dorsolateral prostate (DLP) and cauda epididymis . On the other hand, $TGF-\beta 3$ expression was refractory to the androgen status in and SV but was upregulated 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 $TGF-\beta s$ in an isoform and tissue specific manner.
|Item Type:||Journal Article|
|Additional Information:||Copyright of this article belongs to Society for Endocrinology.|
|Department/Centre:||Division of Biological Sciences > Molecular Reproduction, Development & Genetics (formed by the merger of DBGL and CRBME)|
|Date Deposited:||01 Oct 2007|
|Last Modified:||19 Sep 2010 04:39|
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