Effect of 5alpha-Reductase Inhibitor in Expression of Transforming Growth Factor-beta1 in Benign Prostatic Hyperplasia Patients.
10.4111/kju.2006.47.11.1178
- Author:
Hong Wook KIM
1
;
Je Soo LIM
;
Young Seop CHANG
;
Ki Hak SON
Author Information
1. Department of Urology, Myeonggok Clinical Institute, Konyang University College of Medicine, Daejeon, Korea.
- Publication Type:Original Article
- Keywords:
Benign prostatic hyperplasia;
5alpha-reductase;
Transforming growth factor-beta1
- MeSH:
Apoptosis;
Cell Cycle;
Epithelium;
Humans;
Myocytes, Smooth Muscle;
Peptides;
Phenobarbital;
Prostate;
Prostate-Specific Antigen;
Prostatic Hyperplasia*;
RNA, Messenger;
Signal Transduction;
Transforming Growth Factor beta1;
Transforming Growth Factors;
Transurethral Resection of Prostate
- From:Korean Journal of Urology
2006;47(11):1178-1184
- CountryRepublic of Korea
- Language:Korean
-
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.
