Disease relevance of PGR

• Statistically significant inverse relationships were found between EGF-r and estrogen and progesterone receptor levels in the study of approximately 350 breast cancer patients [1].
• In the mouse mammary tumor virus long terminal repeat that contains four progesterone receptor binding sites, no cooperativity in receptor binding was observed between the single distal and the three proximal sites whereas a low level of cooperativity in receptor binding (about 2-fold) was found between the three proximal sites [2].
• Bovine uterine, cervical and ovarian cytosol estrogen and progesterone receptor concentrations in cystic ovarian disease [3].
• Moreover the rabbit is a suitable species to study the progesterone/progesterone-receptor complex by determining the synthesis of the progesterone-induced protein uteroglobin which may be important in studying endometrial carcinomas [4].
• Progesterone receptor (PR) mRNA was demonstrated in rat parathyroid tissue by in situ hybridization and in human parathyroid adenoma by immunohisto-chemistry [5].

High impact information on PGR

• The results of our study suggest that SH group modifications differentially influence the properties of mammalian PR complexed with either R5020 or RU486 [6].
• Pretreatment of uterine cytosol at 4 degrees C with NEM (4-10 mM) reduced the binding of [3H]RU486 to PR by 40%, but [3H] R5020 binding was completely abolished [6].
• Modulation of calf uterine progesterone receptor (PR), in relation to its binding to synthetic steroids with known agonist (R5020) and antagonist (RU486) properties, was studied in the presence of iodoacetamide (IA), N-ethylmaleimide (NEM), beta-mercaptoethanol (MER), and dithiothreitol (DTT) [6].
• Gonadotropin-Induced Expression of Messenger Ribonucleic Acid for Cyclooxygenase-2 and Production of Prostaglandins E and F2{alpha} in Bovine Preovulatory Follicles Are Regulated by the Progesterone Receptor [7].
• In summary, the LH surge induces expression of PR by granulosa cells and withdrawal from the cell cycle, and these events promote resistance to apoptosis [8].

Chemical compound and disease context of PGR

• Progesterone receptor quantification with radiolabeled promegestone (R 5020) in frozen sections of endometrium and breast cancer tissue [9].

Biological context of PGR

• In vitro, E2-supplementation resulted in an upregulation of PR and ERalpha [10].
• PR and ERalpha mRNA transcripts were elevated in vivo during the follicular phase [10].
• The ERalpha and PR proteins were detected during all physiological states, including lactation [11].
• In addition, ERalpha, ERbeta, PR and ERRalpha were mapped to chromosomes 9, 10, 15 and 29 respectively, by linkage and radiation hybrid mapping [11].
• Progesterone receptor and the cell cycle modulate apoptosis in granulosa cells [8].

Anatomical context of PGR

• Evidence is provided for a varying expression of ERalpha, ERbeta and PR in bovine oviducts at different cycle stages in vivo, respectively under steroid supplementation in vitro [10].
• Chromosomal mapping and quantitative analysis of estrogen-related receptor alpha-1, estrogen receptors alpha and beta and progesterone receptor in the bovine mammary gland [11].
• PR was first detectable in granulosa cells at 10 and 14 h and was not detectable in theca [8].
• Levels of PR mRNA increased in a time-dependent manner in granulosa cells cultured with LH or FSH and in theca cells cultured with LH, peaking at 10 h of culture [12].
• In contrast, PR was localised in the nuclei of epithelial cells in the mammary tIssue of non-pregnant heifers, in primigravid animals, and during late lactation and involution [13].

Associations of PGR with chemical compounds

• Increasing progesterone concentrations were associated with decreased PGR and ESR1 expression [14].
• In agreement with cyclic differences in vivo, estradiol-17beta stimulation increased PGR transcript abundance in BOECs [15].
• Treatment of granulosa cells isolated 14 h after GnRH with the PR antagonist, RU486, induced susceptibility to apoptosis, an effect mediated by PR and not glucocorticoid receptor [8].
• Thermal inactivation of the unoccupied progesterone receptor is inhibited by 10 mM sodium molybdate, whereas thermal inactivation of the ammonium sulfate-purified progesterone receptor is not [16].
• In the E2-treated COCs, ERalpha mRNA was decreased but PR mRNA was upregulated compared with controls [17].

Other interactions of PGR

• Western blot analysis confirmed ESR1 and PGR protein expression throughout the culture period [15].
• Expression and localization of estrogen receptor alpha, estrogen receptor beta and progesterone receptor in the bovine oviduct in vivo and in vitro [10].
• Bovine uterine, cervical and ovarian androgen receptor concentrations. Correlation with estrogen and progesterone receptor concentrations [18].
• We have compared regulation of progesterone receptor (PR) gene expression in MCF-7 human breast cancer cells by cAMP and that by estradiol (E2) and insulin-like growth factor-I (IGF-I) [19].
• By using the progesterone receptor antagonists, RU486 or onapristone, we have shown that this upregulation of the oxytocin gene is mediated by an autocrine loop involving endogenous progesterone and the progesterone receptor in the granulosa cells [20].

Analytical, diagnostic and therapeutic context of PGR

• Expression of ERalpha, ERbeta, PR and ERRalpha was characterized in mammary tissue obtained from multiple stages of bovine mammary gland development using quantitative real-time RT-PCR [11].
• It was found that both ER and PgR responses to SDG ionic strength and the ability of ER to demonstrate temperature-dependent 4S leads to 5S transformation were unimpaired by lyophilization [21].
• Immunohistochemistry also revealed that PR protein was present in both large and small luteal cells [22].
• Interestingly, there was no difference (P >/= 0.05) in P(4) levels after treatment with PR antagonists [22].
• OTR protein was measured by autoradiography with iodinated oxytocin antagonist and ER and PR protein was detected by immunocytochemistry [23].

References