Cell turnover in human seminal vesicles and the prostate: an immunohistochemical study

Citation
J. Pannek et al., Cell turnover in human seminal vesicles and the prostate: an immunohistochemical study, PROSTATE C, 2(4), 1999, pp. 200-203
Citations number
27
Categorie Soggetti
Urology & Nephrology
Journal title
PROSTATE CANCER AND PROSTATIC DISEASES
ISSN journal
13657852 → ACNP
Volume
2
Issue
4
Year of publication
1999
Pages
200 - 203
Database
ISI
SICI code
1365-7852(199907)2:4<200:CTIHSV>2.0.ZU;2-E
Abstract
The human prostate and seminal vesicles are both androgen-dependent sex acc essory organs. Their growth behavior, response to hormone manipulation, sus ceptibility to benign and malignant processes and sex accessory functions, however, differ greatly The growth behavior of most tissues correlates well with the cell turnover rate of that tissue. Therefore, we compared the cel l turnover of normal human prostate and seminal vesicles. Immunohistochemical expression of MIB-1 (proliferation), bcl-2 and transfor ming growth factor (TGF beta) were examined in 20 different samples taken f rom histologically normal human prostatic and seminal vesicle tissue. For t he quantification of apoptosis, the TUNEL technique was used. The apoptosis rates in normal prostatic tissue (0.73 +/- 0.60) were signifi cantly greater (P = 0.003) than those seen in seminal vesicles (0.02 +/- 0. 01). The proliferation rates also differed significantly (P = 0.002) betwee n these tissues (prostate: 0.77 +/- 0.78; seminal vesicles: 0.02 +/- 0.02). Eighty percent of the prostate tissue stained for bcl-2, whereas only 55% of the seminal vesicle tissue showed staining for bcl-2. All seminal vesicl es and 75% of the prostate samples stained for TGF beta. For both androgen-dependent tissues, apoptotic rates closely equaled prolif eration rates. The cell turnover, however, was much higher in the prostate than in the seminal vesicles. TGF beta seems to be more important for the r egulation of cell turnover in the seminal vesicles than bcl-2. These differ ences in the proliferative behavior may explain why disturbances of apoptot ic regulation lead to a more extensive net cell gain in prostatic tissue co mpared to the seminal vesicles. This might help explain the vastly differen t incidence of benign and malignant tumors in these organs.