Disease relevance of ESR1

• These observations showing androgen-induced down-regulation of mammary epithelial proliferation and ER expression suggest that combined estrogen/androgen hormone replacement therapy might reduce the risk of breast cancer associated with estrogen replacement [1].

High impact information on ESR1

• In the current work, we administered RU 486 after 2 weeks of estrogen priming when the oviducts were fully differentiated, the endometrium was in a proliferative state, and ER and PR levels were maximal [2].
• In group I, continuous treatment with E2 maintained a typical proliferative endometrium with abundant Ki-67-positive cells, low levels of apoptosis, and elevated ER and PR; the oviducts were also maintained in a fully ciliated-secretory state [2].
• In that work, RU 486 had been administered at the end of an artificial luteal phase when the oviducts were regressed, the endometrium was in a late secretory state, and estrogen and progestin receptors (ER and PR, respectively) were at minimal levels in both organs [2].
• In group II, P induced a typical progestational secretory state in the endometrium, with few proliferating (Ki-67-positive) epithelial cells, undetectable apoptosis, and decreased ER and PR; as expected, the oviducts were fully regressed, with few Ki-67-positive or ciliated epithelial cells and low levels of ER and PR [2].
• ER alpha mRNA did not change, whereas ER beta decreased 12-36 h after the ovulatory stimulus (P < 0.05) [3].

Biological context of ESR1

• Mifepristone used in EC in the present study resulted in general loss of functional integrity of epithelial compartment characterized by loss of secretory maturation, increased apoptosis and higher degree of degeneration along with decreased expression of VEGF, LIF, PP14 and ER, while PR level increased as compared to control samples [4].
• 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 [5].
• 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 [6].
• Uterine tissues were assayed biochemically for ER content, fixed for histology and frozen for immunocytochemistry of ER with monoclonal antiestrophilins [7].

Anatomical context of ESR1

• These studies show that ER are present constitutively in all cell types of the E-withdrawn (ovariectomized) nonhuman primate uterus, whereas PR are primarily restricted to glandular epithelia [5].
• Ovariectomized monkeys showed positive fluorescence for ER in luminal and glandular epithelia, stromal cells, and smooth muscle cells of the myometrium [5].
• 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].
• E treatment had no effect on ER mRNA in the hypothalamus or pituitary [6].
• Supplemental P treatment decreased ER mRNA in the ventromedial nucleus, but not in the arcuate nucleus or pituitary [6].

Associations of ESR1 with chemical compounds

• Antibodies to ER and PR were obtained from Abbott Laboratories (H222) and Transbio (MPR1) [5].
• The vascular compartment appeared to be compromised along with affected morphological features and decreased expression of VEGF, LIF, ER and PR following the administration of mifepristone [4].
• The regulation of estrogen and progestin receptor (ER and PR, respectively) messenger RNA (mRNA) and protein by their cognate hormones was examined in the hypothalamus and pituitary of steroid-treated monkeys [6].
• Steroid depletion reduced ER alpha mRNA 12 h after hCG, an effect partially reversible by progestin replacement, whereas ER beta mRNA was not affected by steroids [3].
• Steroid regulation of ER and PR mRNA levels in the hypothalamus and pituitary was examined with in situ hybridization [6].

References