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and ß in the Rhesus Monkey Corpus Luteum during the Menstrual Cycle: Regulation by Luteinizing Hormone and Progesterone1
Division of Reproductive Sciences, Oregon Regional Primate Research Center, Beaverton, Oregon 97006
Address all correspondence to: Diane M. Duffy, Division of Reproductive Sciences, Oregon Regional Primate Research Center, 505 NW 185th Avenue, Beaverton, Oregon 97006.
There are conflicting reports on the presence or absence of estrogen
receptor (ER) in the primate corpus luteum, and the discovery of a
second type of estrogen receptor, ERß, adds an additional level of
complexity. To reevaluate ER expression in the primate luteal tissue,
we used semiquantitative RT-PCR based assays and Western blotting to
assess ER
and ß messenger RNA (mRNA) and protein levels in corpora
lutea (n = 3/stage) obtained from adult female rhesus monkeys at
early (days 35), mid (days 68), mid-late (days 1012), and late
(days 1416) luteal phase of the natural menstrual cycle. ER
mRNA
levels did not vary across the stages of the luteal phase, and ER
protein was not consistently detected in luteal tissues. However, ERß
mRNA and protein levels were detectable in early and mid luteal phases
and increased (P < 0.05) to peak levels at
mid-late luteal phase before declining by late luteal phase. To
determine if ERß mRNA expression in the corpus luteum is regulated by
LH, monkeys received the GnRH antagonist antide either alone or with 3
daily injections of LH to simulate pulsatile LH release. Treatment with
antide alone or concomitant LH administration did not alter luteal
ERß mRNA levels. When monkeys also received the 3ß-hydroxysteroid
dehydrogenase inhibitor trilostane to reduce luteal progesterone
production, luteal ERß mRNA levels were 3-fold higher
(P < 0.05) than in monkeys receiving antide + LH
only. Replacement of progestin activity with R5020 reduced luteal ERß
mRNA levels to those seen in animals receiving antide + LH. Thus, there
is dynamic ERß expression in the primate corpus luteum during the
menstrual cycle, consistent with a role for estrogen in the regulation
of primate luteal function and life span via a receptor
(ERß)-mediated pathway. Increased ERß expression in the
progestin-depleted corpus luteum during LH exposure suggests that the
relative progestin deprivation experienced by the corpus luteum between
LH pulses may enhance luteal sensitivity to estrogens during the late
luteal phase of the menstrual cycle.
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