Effect of 5alpha-Reductase Inhibitor in Expression of Transforming Growth Factor-β1in Benign Prostatic Hyperplasia Patients

2006 ◽  
Vol 47 (11) ◽  
pp. 1178
Author(s):  
Hong Wook Kim ◽  
Je Soo Lim ◽  
Young Seop Chang ◽  
Ki Hak Song
Keyword(s):  
Benign Prostatic Hyperplasia ◽  
Growth Factor ◽  
Reductase Inhibitor ◽  
Transforming Growth Factor ◽  
Prostatic Hyperplasia

scholarly journals Transforming growth factor-beta induces growth inhibition and IGF-binding protein-3 production in prostatic stromal cells: abnormalities in cells cultured from benign prostatic hyperplasia tissues

2000 ◽  
Vol 164 (2) ◽  
pp. 215-223 ◽  
Author(s):  
P Cohen ◽  
SE Nunn ◽  
DM Peehl
Keyword(s):  
Benign Prostatic Hyperplasia ◽  
Growth Factor ◽  
Growth Inhibition ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Fold Increase ◽  
Prostatic Hyperplasia ◽  
Igf Binding ◽  
Growth Factor Beta ◽  
Igfbp 3

The IGF axis has been implicated in the pathogenesis of benign prostatic hyperplasia (BPH) via the paracrine action of IGFs and IGF-binding proteins (IGFBPs). In this study, we examined the regulation of cell growth and IGFBP-3 secretion by transforming growth factor-beta (TGF-beta) in prostatic stromal cell (PC-S) cultures from histologically normal tissues and tissues from BPH. PC-S cultures were treated with varying doses of TGF-beta1. Forty-eight hour conditioned media (CM) from these cultures were subjected to Western immunoblotting and ligand blotting for detection and quantification of IGFBPs. IGFBPs-2, -3 and -4 were detected in the CM from normal PC-S cultures. In CM from BPH PC-S, IGFBP-3 levels were 2-fold lower at baseline than in the normal PC-S CM, in addition to the differences in IGFBPs-2 and -5 which we have previously reported. In response to TGF-beta1, a 15-fold increase in the levels of IGFBP-3 was observed in normal PC-S CM, while a mere 2-fold increase was observed in BPH PC-S CM (P<0.001). These findings were confirmed by specific immunoblotting and immunocytochemistry. IGFBP-3 mRNA levels detected by Northern blotting of total RNA extracted from similar cultures showed the induction of IGFBP-3 expression by TGF-beta1 in normal PC-S and its lack of induction in BPH PC-S. Cell growth inhibition in response to TGF-beta1 correlated with the IGFBP-3 concentrations found in CM. Normal PC-S showed a 60% decrease in cell number after 10 days in media with 1 ng/ml TGF-beta1, compared with the untreated control. The decrease in proliferation observed in comparably treated BPH cells was only 20% (P<0.001). In conclusion, BPH PC-S had a reduced IGFBP-3 response to TGF-beta1 and demonstrated decreased TGF-beta1-induced growth inhibition relative to normal PC-S. We hypothesize that in normal PC-S, TGF-beta exerts its anti-proliferative effects by stimulating the production of IGFBP-3, which acts as an inhibitory factor, either by inhibiting IGFs or directly by interacting with cells, and that this process is altered in BPH PC-S.

scholarly journals Fibroblast growth factor receptor 1 (FGFR1) is over-expressed in benign prostatic hyperplasia whereas FGFR2-IIIc and FGFR3 are not

2001 ◽  
pp. 303-310 ◽  
Author(s):  
S Boget ◽  
C Cereser ◽  
P Parvaz ◽  
A Leriche ◽  
A Revol
Keyword(s):  
Growth Factors ◽  
Benign Prostatic Hyperplasia ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Growth Factor Receptor ◽  
Prostatic Hyperplasia ◽  
Fibroblast Growth ◽  
Normal Prostate ◽  
Over Expression

OBJECTIVE: Benign prostatic hyperplasia (BPH) is one of the major public health problems among men: 50% of men over 55 are concerned with this disease. Prostate growth is under the control of androgens which act by means of several growth factors such as fibroblast growth factors (FGFs), epidermal growth factor and transforming growth factor beta. Basic FGF (bFGF) has been shown to stimulate prostatic stromal growth. In BPH, bFGF concentration is two- to threefold higher than in normal prostate. In this work, the bFGF receptors (FGFR1, FGFR2-IIIc and FGFR3) genes expression was evaluated to study the correlation between the expression of bFGF receptors and induction of BPH. METHODS: The expression of FGFRs was analyzed by RT-PCR, FGFR1 was localized by immunohistochemistry and protein expression was evaluated by Western blot. RESULTS: A two- to eightfold over-expression of FGFR1 was observed in BPH compared with normal prostates. FGFR1 was localized in the stroma both in BPH and in normal prostates and 1.5- to 2.5-fold over-expression of the protein was observed. The expression of FGFR2-IIIc and FGFR3, more secondary receptors, was not significantly different between BPH and normal prostates. CONCLUSIONS: bFGF receptors and particularly FGFR1 seem to be involved in the induction and evolution of BPH and probably potentiate bFGF over-expression effects in BPH.

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