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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of estradiol benzoate in the female rat, testosterone propionate in the male rat, and castration in both sexes on specific prolactin binding sites in the particulate membranes of the kidneys and adrenals were studied. Castration resulted in a significant increase in PRL binding activity in the kidneys of both males and females, and in a significant increase in PRL binding activity in the adrenals of the females. The increase in PRL binding with castration and the decrease seen with testosterone treatment were similar in both immature and mature rats. Progesterone administration to castrate females failed to alter PRL binding in both tissues. The present results suggest that estrogen and testosterone participate in the PRL osmoregulatory system in rat.
Steroids 1976 Feb
PMID:Effects of estrogen and testosterone on specific prolactin binding in the kidneys and adrenal of rats. 17 68

We investigated the effects of the peripheral administration of 17 beta-estradiol (E2), estrone (E1), and the catecholestrogens, 2-hydroxyestradiol (2-OHE2) and 2-hydroxyestrone, (2-OHE1), on anterior pituitary gland PRL release in the prepuberal rat. Steroids in oil were injected sc into 25-day-old female and 35- to 40-day-old male rats. The injection of E2, E1, or 2-OHE2, but not of 2-OHE, caused a surge in serum PRL levels in female rats 48 h later, during the afternoon hours. Only E1 induced a PRL surge 24 h after injection. In male rats, the injection of E1 or 2-OHE2, but not of 2-OHE1, elevated serum PRL levels on a chronic basis. The results suggest that 2-OHE1 plays no discernible role in PRL release in either sex, but that 2-OHE2 might play a role in the tonic release of PRL in the male and in the preovulatory release of PRL in the female.
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PMID:Catecholestrogens and release of anterior pituitary gland hormones. II. Prolactin. 627 30

Corpus luteum function in cynomolgus monkeys (Macaca fascicularis) during the menstrual cycle and immediately following parturition was evaluated through in vitro studies on progesterone production by dispersed luteal cells in the presence and absence of human chorionic gonadotropin (hCG) or human prolactin (hPRL). Luteal cells isolated between days 17-20 of the menstrual cycle secreted progesterone (P) during short-term incubation (21.6 +/- 1.2 ngP/ml/5 X 10(4) cells/3 hr, X +/- S.E., n = 7) and responded to the addition of 1-100 ng hCG with a significant (p less than 0.05) increase in P secretion. Cells removed the day of delivery secreted large, but variable (27.9-222 ng/ml, n = 4) amounts of P during short-term incubation. Moreover, hCG (100 ng/ml) stimulation of P production by cells at delivery (176 +/- 19% of control) was less than that of cells from the cycle of (336 +/- 65%). The presence of hPRL (2.5-5000 ng/ml) failed to influence P secretion by luteal cells during short-term incubation in the presence or absence of hCG. P production by luteal cells obtained following delivery declined markedly during 8 days of culture in Ham's F10 medium: 10% fetal calf serum. Continual exposure to 100 ng/ml of hCG or hPRL failed to influence P secretion through Day 2 of culture. Thereafter hCG progressively enhanced (p less than 0.05) P secretion to 613% of control levels at Day 8 of culture. In contrast, hPRL significantly increased P secretion (163% of control levels, p less than 0.05) between Day 2-4 of culture, but the stimulatory effect diminished thereafter. The data indicate that dispersed luteal cells from the cynomolgus monkey provide a suitable model for in vitro studies on the primate corpus luteum during the menstrual cycle, pregnancy, and the puerperium, including further investigation of the possible roles of gonadotropin and PRL in the regulation of luteal function in primates.
Steroids 1980 May
PMID:Progesterone production by luteal cells isolated from cynomolgus monkeys: effects of gonadotropin and prolactin during acute incubation and cell culture. 677 95

The signaling mechanisms of estrogens interact with those of growth factors to control the pituitary gland functions. The contribution of the membrane bound estrogen receptor in these actions is not fully understood. In this study, we focused on the regulatory action of estradiol in interaction with insulin on the secretory and proliferative lactotroph cell activities from primary pituitary cell cultures. Furthermore, we studied the involvement of ERK1/2, PKC epsilon and Pit-1 in these actions. In serum free conditions, estradiol and estradiol-BSA promoted a differential secretory activity on PRL cells but were unable to induce lactotroph cell proliferation. However, both free and conjugated estradiol were competent arresting the mitogenic activity promoted by insulin. Estradiol, estradiol-BSA and insulin stimuli increased the PKC epsilon, phosphorylated ERK 1/2 and Pit-1 expression, although combined treatments with estradiol/insulin or estradiol-BSA/insulin induced a significant reduction in these levels, in close correlation with the decrease of lactotroph cell proliferation. The pre-treatment with PKC inhibitor BIM significantly inhibited the ERK activation promoted by insulin without modifying the ERK expression levels induced by estradiol or estradiol-BSA. By immuno-electron-microscopy the alpha nuclear estrogen receptor was localized in the plasma membrane of lactotroph cells. These findings suggest that the membrane bound ER participates modulating lactotroph cells proliferation via PKC epsilon, ERK1/2 and Pit-1. The interactions between estradiol and growth factors, inducing both mitogenic and antimitogenic effects, could provide glandular plasticity preventing an over-proliferation induced by growth factors.
Steroids 2008 May
PMID:Estradiol interacts with insulin through membrane receptors to induce an antimitogenic effect on lactotroph cells. 1828 21

Progesterone (P4) has controversial physiological effects on the regulation of the lactotroph population. While some studies have shown a negative role for P4 in prolactin secretion and lactotroph proliferation, antagonizing estradiol effects, others demonstrated a proliferative role of P4 at the pituitary level. Usually, progesterone actions in the pituitary gland were studied through their classical, genomic pathways triggered by nuclear progesterone receptors (nPRs). However, in 2003, the scene became more complex with the discovery of another group of progesterone receptors involved in rapid, non-genomic P4 effects: the membrane progesterone receptors (mPRs), which are members of the progesterone and adipoQ receptor (PAQR) family. This review examines the historical background and current data on the study of progesterone actions on PRL secretion providing new evidence of P4 effects at the hypothalamic and at the pituitary level through non-classic P4-receptors. In addition, we explore the role of progesterone in the development of experimental prolactinomas, a controversial topic in the literature.
Steroids 2019 12
PMID:New insights into progesterone actions on prolactin secretion and prolactinoma development. 3152 9