Ontogeny and Regulation of a Rat Placental Estrogen Receptor*

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Abstract
Scatchard analysis of cytosol and nuclear fractions of rat placental homogenates under exchange conditions showed that an estrogen receptor (RE) was present at high levels during a limited period of midpregnancy in the basal zone of the placenta. The disappearance of placental RE appeared to be under strict regulation. From days 9-15 of pregnancy (day 0 = sperm-positive day) cytosol RE fell from 30,000 to 600 sites/cell and nuclear RE from 3400 to 200 sites/cell. It was attempted to change RE levels from days 12-15 by manipulating hormone levels and/or increasing the proportion of trophoblast giant cells in the basal zone of the placenta. Two effects on RE levels could be achieved. The disappearance of cytosol RE was delayed by 2 days under experimental conditions in which estrogen was lowered by ovariectomy. The temporarily increased levels of cytosol RE may have been due to insufficient estrogen to translocate RE into the nucleus rather than to increased synthesis of RE, inasmuch as RE fell to low levels on day 15 as in normal pregnancy. The loss of nuclear RE was accelerated by 2 days under experimental conditions in which rats with their own ovaries received exogenous estrogen and progesterone. The accelerated loss may have been caused by a combination of higher than normal levels of estrogen and progesterone, higher estrogen acting to translocate increased amounts of RE into the nucleus and elevated progesterone acting to interfere with the replenishment of RE in the cytosol. A relative preponderance of trophoblast giant cells caused by fetectomy did not affect the RE levels or rate of disappearance, possibly because progesterone secreted by the trophoblast giant cells before fetectomy (on day 12), had already determined the rate of RE loss by its interference with RE replenishment.