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Content of Nuclear Estradiol Receptor Complex in Rat Corpora Lutea During Pregnancy: Relationship to Estrogen Concentrations and Cytosol Receptor Availability¹

Reproductive Endocrinology Program, Department of Pathology, University of Michigan Ann Arbor, Michigan 48104

Abstract

The content of estradiol receptor in cytosol and nuclear cell fractions of rat corpora lutea changed during pregnancy. The binding of [³H]estradiol to luteal cell cytosol was high early in pregnancy between days 3–11, decreased on days 12 and 15 and was low throughout the remainder of pregnancy. In contrast, the binding of [³H]estradiol to nuclear receptor, as measured by nuclear exchange assay, was low early in pregnancy, increased between days 10–15, remained high through day 18 and decreased on days 20 and 22. The administration in vivo of estradiol-17β(40 µg) 1 hr prior to sacrifice stimulated an increase in nuclear receptor content early in pregnancy (days 3, 6, 8, 10-12) butnot later in pregnancy (days 15, 18, 20 and 22). These results suggested that the estradiol binding component(s) present in rat luteal cell cytosol early in pregnancy represented available estradiol receptor capable of being translocated to the nucleus in the presence of sufficient estradiol. However, once available receptor has been saturated by endogenous hormone at midgestation, exogenous hormone has no further effect on nuclear receptor content. Importantly, loss of nuclear receptor content late in pregnancy appears to reflect decreased levels of total cellular receptor indicating that corpora lutea at the end of pregnancy have lost the primary mechanism for responding to estrogens. Thus, various stages of luteal cell differentiation are associated with changes in the intra-cellular distribution and total cellular content of estradiol receptor suggesting that luteal cell function may be regulated selectively and separately by hormone concentrations and hormone receptor availability.(Endocrinology 96:227, 1975).

Footnotes

¹ Supported in part by a Program Project Grant in Reproductive Endocrinology from the National Institutes of Child Health and Human Development NIH-HD-05318) and by a training grant from the Ford Foundation.

² Supported by a Postdoctoral Fellowship in Reproductive Biology from the Rockefeller Foundation.

Received June 10, 1974.

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