Ja. Sensibar et al., Differential growth rates in stromal cultures of human prostate derived from patients of varying ages, PROSTATE, 38(2), 1999, pp. 110-117
BACKGROUND. This study was undertaken to attempt to characterize changes in
in vitro growth rates and cellular phenotypes of human prostatic stroma as
sociated with aging and/or development of benign prostatic hyperplasia (BPH
).
METHODS. Prostate stromal cell strains were established from 12 tissue dono
rs of varying age. Culture growth rate was determined by cell counts over a
6-day period. Cell phenotype was assessed by immunocytochemical staining f
or smooth muscle alpha-actin, smooth muscle myosin, and prolyl-4-hydroxylas
e.
RESULTS. Growth rates of prostate stromal strains in vitro varied. Stromal
cells derived from aged males with BPH had significantly slower growth rate
s than cells from younger donors. A positive reaction for prolyl-4-hydroxyl
ase, a mesenchymal cell marker, was present in all cell cultures regardless
of donor age. Expression of smooth muscle-specific actin, a nonspecific sm
ooth muscle cell marker, was present in 48-79% of prostate stromal cultures
. Staining for smooth muscle myosin, a specific smooth muscle cell marker,
was found to vary significantly with age. The percentage of smooth muscle m
yosin-positive cells derived from males aged 15, 45, 57, and 72 years were
0.70 +/- 0.14%, 2.12 +/- 0.30%, 4.20 +/- 0.89%, and 26.25 +/- 1.0%, respect
ively. The shape and size of actin- and/or myosin-positive stromal cells fr
om a 72-year-old donor culture were also usually larger and polygonal in sh
ape as compared to thin and elongated shapes in 15-year-old donor cultures.
The shape of actin- and/or myosin-positive cells from a 45-year-old donor
culture demonstrated both phenotypes.
CONCLUSIONS. These results suggest that in human prostate stromal cells cul
tured as described, the growth rate decreases, the percent of smooth muscle
cells increases, and the cellular shape changes with increasing donor age
and or/development of BPH. (C) 1999 Wiley-Liss, Inc.