ABSTRACT
Purpose: Transforming growth factor (TGF)-beta is a member of the superfamily of polypeptides, which control cell cycle progression and a variety of other cellular activities. TGF-beta1 has been implicated as an effector of the induction of apoptosis in response to 5alpha-reductase inhibitor (5ARI) and; therefore, causes a decrease in the prostate volume. We investigated the effect of 5ARI in the expression of TGF-beta1 in benign prostatic hyperplasia (BPH). Materials and Methods: 50 patients diagnosed with BPH were divided into two groups. The control group (n=30), in which a transurethral resection of the prostate (TURP) was performed without medication, and the 5ARI group (n=20), who were administrated with 5 mg of 5ARI daily for at least 3 months, followed by TURP. The resected specimens were stained with anti-rabbit TGF-beta1 polyclonal antibody using immunofluoroscent staining. The expression of TGF-beta1 was analyzed with a confocal laser scanning microscope and an image analyzer. The mRNA level of TGF-beta1 was determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Results: There were no statistical differences in the patient characteristics, including age, serum prostate-specific antigen (PSA) level and prostate volume, between the two groups. The expression of TGF-beta1 was demonstrated in the luminal epithelium and smooth muscle cells in BPH. TGF-beta1 was more strongly expressed in the luminal epithelium of both groups, and in the 5ARI group than the control (p<0.001). Conclusions: These results suggest that 5ARI up-regulates the expression of TGF-beta1 in BPH patients, and may a play role as an inhibitor in the proliferation of BPH through the TGF-beta1 signal pathway.