Endometrial stromal differentiation (decidualization) is essential for
implantation of the developing blastocyst. Because prostaglandins (PG
s) are synthesized in the endometrium, and PG-binding sites have been
demonstrated in the proliferative endometrial stromal cell (the precur
sor of the decidual cell), experiments were performed to determine whe
ther PGs are involved in the process of decidualization. Human endomet
rial stromal cells were cultured for 18 days in Dulbecco's Modified Ea
gle's Medium-2% fetal bovine serum with 1 mu M medroxyprogesterone ace
tate (MPA) and 10 nM estradiol, with and without PGE(2) or PGF(2 alpha
), Expression of PRL was used as a marker of decidualization. In the p
resence of estradiol and MPA alone (control), PRL was detected beginni
ng on day 9 and gradually increased through day 18. In contrast, PRL w
as detected on day 3 in the PGE(2)-treated cells, and the magnitude of
stimulation in these cells on days 9-12 was 1300-1400% of that in con
trol cells. Furthermore, the PRL mRNA content of the PGE(2)-treated ce
lls on day 12 was 4.6-fold greater than that in the control cells. The
effect of PGE(2) on PRL production was dose dependent, with a minimal
effective dose of 10(-10) M. PGE(2) in the absence of steroids had a
minimal effect on PRL production. In contrast to PGE(2), PGF(2 alpha),
treatment had no effect on PRL expression in steroid-treated cells. T
hese results indicate that there are synergistic effects among PGE(2),
estradiol, and MPA, resulting in acceleration of endometrial stromal
cell differentiation and enhanced PRL expression.