Comparison of tritium-labeled steroids for progesterone receptor assay in human endometrium.
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Biomedical subjects
Publications and source records attributed to N Ide.
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Steroid receptors in endometriosis and adenomyosis were investigated to clarify their clinical significance. The receptor levels were determined by Scatchard plot analysis (4 degrees C, by dextran-coated charcoal). In the cytosols of both tissues, the 17 beta-estradiol-estrogen receptor (ER) complex demonstrated a dissociation constant (Kd) of 4.5 x 10(-10) M; the Kd of the progesterone-progesterone receptor (PR) complex was 1.5 x 10(-9) M; and the Kd of the dihydrotestosterone-androgen receptor (AR) complex was 4.0 x 10(-10) M. Seven cases of ovarian endometriosis were studied. The ER and PR levels in endometriosis seemed to be lower than those in the corresponding normal endometrium. AR was also present. There was a suggestion that most endometriosis is least responsive to progestogens. Ten cases of adenomyosis were studied. Histologic dating revealed a delay in the most aberrant endometrial tissue in adenomyosis, as compared with dating of corresponding normal endometrial tissue. ER and AR were detected in all cases. PR was not detected in some cases and, when detected, the content seemed to be lower, possibly suggesting the delayed dating.
This study was designed to investigate the chromatin transcription in vitro by progesterone-receptor complex in the estrogen-primed rabbit uterus. RNA synthesis by the uterine chromatin was stimulated when progesterone-uterine cytosol complex was bound to the chromatin and the stimulation was dependent upon the dose of the bound progesterone-cytosol 8S complex and upon the incubation time of the complex in the presence of the chromatin. Either norethindrone- or dydrogesterone-uterine cytosol complex also stimulated the uterine chromatin transcription but the extent was less than that of progesterone complex. These results indicate that progesterone as well as synthetic progestogens can directly regulate chromatin transcription via progesterone receptor in the rabbit uterine cells.
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