Peyronie's disease is a fibromatosis of the tunica albuginea which affects
up to 2% of men. Plaque development is believed to result, at least in part
, from fibroblast proliferation and excess collagen deposition. Numerous or
al and intralesional therapies have been used, including verapamil, colchic
ine and steroids. The purpose of this study was to investigate the in vitro
effects of prostaglandin-E1 (PGE1), verapamil and colchicine on the prolif
eration rates of fibroblasts derived from Peyronie's disease tissue.
Using tissue culture, multiple cell lines comprising fibroblasts from Peyro
nie's plaque, normal tunica and foreskin were established. Cells of low pas
sage were removed from the parent culture and incubated with varying concen
trations of PGE1 (0.1-10 mg/ml), verapamil (10-1000 mg/ml), and colchine (2
.5 mg/ml). Proliferation was assessed at 48, 72 and 96 hours using the Vybr
ant(TM) MTT cell proliferation and then compared to control cells.
Six plaque lines and 5 normal tunical cell lines were established. These ce
ll lines exhibited excellent linear growth in culture media alone. Co-cultu
re with PGE1 resulted in no significant inhibition at 0.1 and 1 mg/ml, but
a mean inhibition of 60.6 +/- 11.5% at a concentration of 10 mg/ml was note
d. Similar inhibition was noted with verapamil at 100 and 1000 mg/ml with a
mean inhibition of 65.2 +/- 10.6%. Colchicine resulted in a mean inhibitio
n of 28% at a concentration of 2.5 mg/ml. Maximum inhibition occurred at 96
hours in all cases. There was no statistically significant difference in p
roliferation rates between plaque and normal tunical cell lines.
We have developed an in vitro model to assess the effects of biologically a
ctive agents on the growth of fibroblasts derived from Peyronie's disease t
issue. Our data suggests that PGE1, verapamil, and colchicine inhibit in vi
tro proliferation of fibroblasts at specific concentrations. Refinement and
application of this knowledge may allow the development of useful pharmaco
logic strategies for men with PD.