Regressive changes in finasteride-treated human hyperplastic prostates correlate with an upregulation of TGF-Beta receptor expression
Abstract: doi.wiley.com/10.1002/(SICI1097-0045(19981001)37:2%3C84::AID-PROS4%3E3.0.CO;2-L
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BACKGROUND
Prostatic atrophy has been documented histologically as a consequence of finasteride action on human hyperplastic prostates. An increase in apoptotic rates has also been reported in androgen-deprived hyperplastic prostates.
Transforming growth factor beta (TGF-B) signaling is implicated in apoptotic cell death. TGF-Bs have been detected in normal and diseased human prostate. In the normal prostate, TGF-B acts as a predominantly negative growth regulator. TGF-B signaling receptors TBRI and TBRII have been shown to be negatively regulated by androgens.
METHODS
We studied the histological changes in 9 selected finasteride-treated patients with benign prostatic hyperplasia (BPH), and analyzed the levels of expression and localization of TGF-B receptor types TBRI and TBRII in these patients as compared to selected BPH controls.
RESULTS
The prostatic epithelial compartment seemed to be a primary target site for finasteride action, since we observed moderate to severe glandular atrophy after 4-6 months of treatment. TGF-B receptors were upregulated in treated cases.
We assessed a twofold increase in TBRII mRNA levels in treated cases as compared to controls. An increase in both TBRI and TBRII at the protein level by immunostaining was observed, which also provided a helpful means for detecting glands undergoing regression.
CONCLUSIONS
We conclude that finasteride may modulate the TGF-B signaling system to promote changes leading to apoptosis of epithelial cells and prostatic glandular atrophy.
Prostate 37:84-90, 1998. © 1998 Wiley-Liss, Inc.