Routine analysis of E2 and progesterone levels revealed an unexpected
and interesting result (Fig. 3): the serum E2 level at 5.5
dpc in the VED group was more than twice that of the control group(P < 0.01) and gradually decreased by 7.5 and 9.5 dpc to a level that
was similar to the control group. However, levels of progesterone
did not differ between the two groups and remained constant over
the entire experimental time course. Because decidualization is
presumably initiated at the time of expected implantation, around
5.5 dpc, this observation implies that E2 is highly likely to play an
important role in initiating the process of spontaneous decidualization.
Some earlier studies have reported increased levels of
serum E2 during the implantation period and speculated that the E2surge may participate in endometrial decidualization [16,17]. In the
1960s, Shelesnyak found that 30% of pseudopregnant rats injected
with low-dose E2 exhibited spontaneous decidualization [18].
Furthermore, administration of an anti-estrogen, ethamoxytriphetol,
on day 3 of pregnancy, or pseudopregnancy, prevented
decidualization and interfered with implantation [18]. The E2 surge
is required during the period of progesterone predominance and
differs in function from the estrogen required to prime the uterus
for proliferation. However, the degree of decidualization in the
current VED group was greater than that of rats receiving low-dose
E2 injection in a previous study [18]. Consequently, it is possible
that the E2 surge at 5.5 dpc may be one of the reasons that our VED
rats experienced spontaneous decidualization.