Rabbit endometrial and myometrial cytosolic estrogen receptors
Numerous studies have been conducted into function, structure and mode of action of steroid receptors. Research has led to a partial understanding of interactions of receptors with hormones and the function of combined hormone-receptor complexes as inducers of transcriptional events. Despite investigation into those functions of receptors, little information is available on the significance of changes in receptor levels during different stages of the estrous cycle or pregnancy. Virtually none has been accumulated on the character of receptors found in isolated endometrial and myometrial uterine tissues. This study was initiated to test the hypothesis that endometrial and myometrial estrogen receptors of the rabbit respond differently to hormonal stimulation.
Changes in estrogen receptors were observed during the course of early pregnancy and under stimulation by steroid hormone: Estrogen receptor affinity (Kα) and titers were highest in the endometrium on day 4 of pregnancy. Kα reached 2.69(±0.29)x109 and titers reached 13.35 ± 0.45 fmol(ugP/ugDNA)-1. Peak values for myometrial receptor affinity (2.43± 0.42 x 109M-1 and titers (5.34 ± 1.08 fmol(ugP/ugDNA)-1) occurred on day one of pregnancy. Endometrial titers were significantly different from myometrial titers from day three of pregnancy onwards. Receptor titers in implantation-sites were reduced between day (7.98 ± 1.66 fmol(ugP/ugDNA)-1) amd day nine (3.47 ± 0.59 fmol(ugP/ugDNA)-1) of pregnancy.
Seasonal changes in estrogen receptor Kα but not in titer were observed. Lowest values occured in early spring (0.259±0.065x109M-1) and highest values were observed in the fall (2.21 ± 0.21 x 109M-1).
Seasonality had not been anticipated in this species.
Estrogen treatment of ovariectomized animals resulted in reduction of Kα and titer over oil treated controls. Endometrial Ka was depressed by 48%, and endometrial titer by 86%. Ka of the myometrium decreased by 84%, and titer was reduced by 86%. Progesterone treatment decreased titers to a less appreciable extent (44% in endometrium and 75% in myometrium) and depressed affinity only in the myometrium (25%). Changes in affinity were probably caused by the presence of a competitive inhibitor which was present in the cytosol after steroid treatment.
This study served to demonstrate a difference in endometrial and myometrial estrogen receptor. In addition, an unexpected seasonal variation in receptor-hormone interaction was described. As a result of the data obtained, a model for control of receptor affinity was proposed. Modifications in titer and affinity might govern responsiveness of cytoplasmic estrogen receptor.
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