Disease relevance of PR

• Tamoxifen induced ER and PR but not Ki-67 expression or glandular hyperplasia [1].

High impact information on PR

• These results suggest that E2 and P replacement decreases coronary artery reactivity through direct interactions with ER and PR in coronary artery VMC [2].
• In vivo treatment of ovx monkeys with E2 tended to up-regulate PR in VMC, but MPA appeared to down-regulate PR expression [2].
• PR were localized to coronary artery VMC and interstitial cell nuclei [2].
• Steroid concentrations in venous blood, coronary artery estrogen receptor (ER) and progesterone receptor (PR) localization, and isolated vascular muscle cell (VMC) Ca2+ and protein kinase C responses to serotonin and U46619 (a thromboxane A2 mimetic) were measured [2].
• In order to determine whether these effects involve receptor-mediated mechanisms, we have examined the concentration and distribution of estrogen receptor (ER), androgen receptor, and progesterone receptor (PR) in the adrenal glands of fetal, immature, and adult rhesus monkeys [3].

Biological context of PR

• Immunofluorescent analyses of E receptor (ER) and PR were performed on fresh frozen cryostat sections (6 microns) of uterine tissue from ovariectomized (3 months) and estradiol (E2)-treated (peak level of E2 during an artificial menstrual cycle) rhesus monkeys [4].
• E2 treatment, which simulated the follicular phase and E2 surge, resulted in the appearance of immunofluorescent PR in luminal epithelia, stromal cells, and myometrial smooth muscle cells [4].
• Although these observations suggest diverse cell-specific regulatory mechanisms, they are consistent with ER- and PR-mediated physiological events, such as PRL secretion and sexual behavior [5].
• P regulation of luteal PR mRNA was investigated by administering trilostane, a 3 beta-hydroxysteroid dehydrogenase inhibitor, to female rhesus macaques beginning on day 6 or 7 of the luteal phase, which reduced serum P until the time of lutectomy [6].
• Females were found to have approximately 30% more PR-labeled cells compared with males throughout the DRN (P < 0.05), but no sex difference was detected in the number of neurons demonstrating ER-ir [7].

Anatomical context of PR

• E treatment induced PR mRNA in the medial basal hypothalamus and pituitary [5].
• These studies serve to define the cellular pattern of E2-induced PR in the primate uterus [4].
• After E2 treatment strong positive fluorescence for PR was observed in luminal and glandular epithelia, stromal cells, and myometrial smooth muscle cells [4].
• In contrast, positive fluorescence for PR was observed primarily in glandular epithelia, with little or no fluorescent detection in luminal epithelium, stromal cells, or myometrial smooth muscle cells [4].
• It has been suggested that in prenidatory stage rhesus monkey endometrium elevated concentrations of nuclear ER and PgR possibly indicate higher degree of nuclear occupancy required for endometrial differentiation permitting blastocyst implantation [8].

Associations of PR with chemical compounds

• Estrogen (E) has been shown to induce an increase in progesterone (P) receptor (PR) concentration in uterine tissue of both rodents and primates [4].
• Because of the presence of different cell types within the uterus, we were interested in determining whether estrogen-induced PR were cell type specific in the nonhuman primate uterus (rhesus monkey) [4].
• Steroid regulation of ER and PR mRNA levels in the hypothalamus and pituitary was examined with in situ hybridization [5].
• PR mRNA was reduced by steroid depletion throughout the periovulatory interval (P < 0.05); however, progestin replacement returned PR mRNA to control levels at 12 h [9].
• Antibodies to ER and PR were obtained from Abbott Laboratories (H222) and Transbio (MPR1) [4].

Other interactions of PR

• However, P has no significant effect on PR expression in the hypothalamus even though P decreases ER in the ventromedial nucleus [5].
• The distribution of androgen receptor was similar to that of ER, whereas there was no detectable staining for PR in the adrenals of either adult or fetal animals [3].

Analytical, diagnostic and therapeutic context of PR

• There was excellent agreement with PR protein detection by immunocytochemistry [5].
• The distribution of estrogen receptors (ER), progesterone receptors (PR), PRL, and gonadotropins in different cell types of the monkey pituitary was examined by immunocytochemical (ICC) labeling of pituitary cell cultures [10].
• Progesterone receptor isoforms were identified and quantified by Western blot analysis, and PR mRNA was determined by a specific ribonuclease protection assay [11].

References