Based on morphology, it has been suggested that prostaglandin E2 (PGE2
) accelerates the process of endometrial stromal cell differentiation
to decidual cells in the rat. The present study investigated this poss
ibility, using changes in uterine weight and in endometrial alkaline p
hosphatase (ALP) activity as indicators of decidualization. Rats were
ovariectomized and treated with one of two steroid protocols; the firs
t was identical to that previously used for the study of morphology, t
he second a modified protocol which results in greater uterine sensiti
zation for decidualization, producing larger amounts of decidual tissu
e, thereby making it easier to detect differences between treatments.
On the day of uterine sensitization, rats within each treatment protoc
ol were given a unilateral intrauterine infusion of phosphate-buffered
saline (PBS) or PGE2 plus indomethacin, and killed 24, 48 or 72 h lat
er. The time-courses for the increases in uterine weight and ALP activ
ity in uterine horns infused with PBS or PGE2 plus indomethacin differ
ed between steroid protocols, but within a protocol were statistically
indistinguishable. The results do not support the hypothesis that PGE
2 accelerates the process of decidualization but do provide additional
support for the notion that PGE2 is a physiological rather than pharm
acological mediator of decidualization.