Prostate Growth Factor: Characterization and its Role in Normal Prostate and in Benign Prostatic Hyperplasia

1989 ◽  
pp. 29-48
Author(s):  
Michael T. Story
Keyword(s):  
Benign Prostatic Hyperplasia ◽  
Growth Factor ◽  
Prostatic Hyperplasia ◽  
Normal Prostate ◽  
Prostate Growth

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.

scholarly journals Targeting Stromal Androgen Receptor Suppresses Prolactin-Driven Benign Prostatic Hyperplasia (BPH)

2013 ◽  
Vol 27 (10) ◽  
pp. 1617-1631 ◽  
Author(s):  
Kuo-Pao Lai ◽  
Chiung-Kuei Huang ◽  
Lei-Ya Fang ◽  
Kouji Izumi ◽  
Chi-Wen Lo ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Benign Prostatic Hyperplasia ◽  
Prolactin Receptor ◽  
Prostatic Hyperplasia ◽  
Proliferation Index ◽  
Normal Prostate ◽  
Prostate Hyperplasia ◽  
Prostate Cancer Development ◽  
Underlying Mechanisms ◽  
Prostate Growth

Stromal-epithelial interaction plays a pivotal role to mediate the normal prostate growth, the pathogenesis of benign prostatic hyperplasia (BPH), and prostate cancer development. Until now, the stromal androgen receptor (AR) functions in the BPH development, and the underlying mechanisms remain largely unknown. Here we used a genetic knockout approach to ablate stromal fibromuscular (fibroblasts and smooth muscle cells) AR in a probasin promoter-driven prolactin transgenic mouse model (Pb-PRL tg mice) that could spontaneously develop prostate hyperplasia to partially mimic human BPH development. We found Pb-PRL tg mice lacking stromal fibromuscular AR developed smaller prostates, with more marked changes in the dorsolateral prostate lobes with less proliferation index. Mechanistically, prolactin mediated hyperplastic prostate growth involved epithelial-stromal interaction through epithelial prolactin/prolactin receptor signals to regulate granulocyte macrophage-colony stimulating factor expression to facilitate stromal cell growth via sustaining signal transducer and activator of transcription-3 activity. Importantly, the stromal fibromuscular AR could modulate such epithelial-stromal interacting signals. Targeting stromal fibromuscular AR with the AR degradation enhancer, ASC-J9®, led to the reduction of prostate size, which could be used in future therapy.

Transforming Growth Factor β and its Receptor Types I and II. Comparison in Human Normal Prostate, Benign Prostatic Hyperplasia, and Prostatic Carcinoma

1998 ◽  
Vol 16 (2) ◽  
pp. 101-110 ◽  
Author(s):  
Mar Royuela ◽  
María P. De Miguel ◽  
Fermín R. Bethencourt ◽  
Manuel Sanchez-Chapado ◽  
Benito Fraile ◽  
...  
Keyword(s):  
Benign Prostatic Hyperplasia ◽  
Growth Factor ◽  
Prostatic Carcinoma ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Prostatic Hyperplasia ◽  
Normal Prostate
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