Placental Growth factor: another piece in the BPH jigsaw?
BAUS ePoster online library. Devlin C. 06/26/19; 259495; P13-10
Mr. Conor Devlin
Mr. Conor Devlin
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Abstract
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INTRODUCTION

Benign prostatic hyperplasia (BPH) is a common disease, whose pathogenesis is not fully understood, although a number of growth factors (GFs) produced by prostate epithelial and stromal layers may play key roles. Current treatments take little account of GF-induced cell proliferation. By studying GF gene expression in enriched prostate cell subtypes we have now identified multiple novel GFs which influence BPH pathogenesis.

Materials and methods

Prostate cell subtypes were enriched directly from fresh BPH biopsies (TURP). GF mRNA array analysis was performed on six BPH samples. Placental growth factor (PGF) protein and receptor expression was validated using western blotting on tissue homogenates, immunocytochemistry on fixed cell subtypes and immunohistochemistry on tissue array samples.

RESULTS

PGF mRNA expression in BPH was more than double that of normal prostate cells. Within BPH tissue, PGF expression was 66 times higher within the stromal population, compared to the epithelial layer. PGF was expressed at the protein level in all homogenate samples. In fixed cells, PGF expression was highest within stromal cells. Interestingly, using formalin fixed tissue arrays, PGF expression was most abundant within the luminal cells, whilst also observed within the stroma. In all preparations, the principal PGF receptor - vascular endothelial growth factor receptor 1 (VEGFR1) was detectable in each cell subtype.

Conclusions

PGF appears to be an important GF in BPH, providing a potential paracrine mechanism for the maintenance of the disease, perhaps mediated by stromal cells. Growth factor receptors could provide a novel source of next-generation, rationally targeted BPH treatments.
INTRODUCTION

Benign prostatic hyperplasia (BPH) is a common disease, whose pathogenesis is not fully understood, although a number of growth factors (GFs) produced by prostate epithelial and stromal layers may play key roles. Current treatments take little account of GF-induced cell proliferation. By studying GF gene expression in enriched prostate cell subtypes we have now identified multiple novel GFs which influence BPH pathogenesis.

Materials and methods

Prostate cell subtypes were enriched directly from fresh BPH biopsies (TURP). GF mRNA array analysis was performed on six BPH samples. Placental growth factor (PGF) protein and receptor expression was validated using western blotting on tissue homogenates, immunocytochemistry on fixed cell subtypes and immunohistochemistry on tissue array samples.

RESULTS

PGF mRNA expression in BPH was more than double that of normal prostate cells. Within BPH tissue, PGF expression was 66 times higher within the stromal population, compared to the epithelial layer. PGF was expressed at the protein level in all homogenate samples. In fixed cells, PGF expression was highest within stromal cells. Interestingly, using formalin fixed tissue arrays, PGF expression was most abundant within the luminal cells, whilst also observed within the stroma. In all preparations, the principal PGF receptor - vascular endothelial growth factor receptor 1 (VEGFR1) was detectable in each cell subtype.

Conclusions

PGF appears to be an important GF in BPH, providing a potential paracrine mechanism for the maintenance of the disease, perhaps mediated by stromal cells. Growth factor receptors could provide a novel source of next-generation, rationally targeted BPH treatments.
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