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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen has been shown to increase proenkephalin (PE) mRNA levels in neurons of the ventrolateral aspect of the ventromedial hypothalamic nucleus (VL-VM). In this series of experiments, we examined the temporal qualities of this induction by determining both the latency of the estrogen-induced elevation in PE mRNA levels and the rate at which the message levels decline following removal of estrogen. In addition we have examined the effects of progesterone on PE gene expression in the VL-VM of estrogen-primed rats. The latency of the estrogen-induced elevation in PE mRNA levels was found to be relatively short: PE mRNA levels were increased 2-fold within 1 h of estrogen replacement. Following estrogen removal the levels of PE mRNA declined rapidly. Progesterone treatment attenuated this decline, prolonging the estrogen-induced elevation of PE mRNA levels. These results suggest that estrogen rapidly increases PE mRNA levels through a mechanism that probably involves alterations in both the rate of appearance and the rate of degradation of the message. Together, the short latency of the estrogen-induced elevation and the rapid rate of decay following estrogen removal indicate that PE gene expression is highly sensitive to fluctuating estrogen levels. The effect of progesterone suggests that this enkephalinergic system may be regulated by both estrogen and progesterone during the estrous cycle.
Brain Res Mol Brain Res 1989 Jan
PMID:Estrogen regulation of proenkephalin gene expression in the ventromedial hypothalamus of the rat: temporal qualities and synergism with progesterone. 292 83

Treatment of 3T3-L1 preadipocytes (fibroblasts) with 250 nM dexamethasone for 48 hr caused a doubling of total beta-adrenergic receptors and an increase in beta 2-adrenergic receptor subtype proportion from approximately 50% in controls to 85% in treated cells. The responses to epinephrine and norepinephrine in a whole cell cAMP accumulation assay reflected these changes. The effects of dexamethasone on beta-adrenergic receptors were mediated through the glucocorticoid receptor and were time and dose dependent with an EC50 of 2.77 +/- 0.73 nM for an increase in the proportion of beta 2-adrenergic receptors. The rank order of potency of steroids to effect these changes (betamethasone = dexamethasone greater than fludrocortisone greater than hydrocortisone = triamcinolone greater than aldosterone) correlated with their glucocorticoid potency. [3H]Dexamethasone binding to intact cells yielded a KD value of 3.47 +/- 0.38 nM for binding to the glucocorticoid receptor which correlated well with the EC50 for dexamethasone to alter beta-adrenergic receptors. Inhibition of [3H]dexamethasone binding by other steroids confirmed that the ability of steroids to regulate beta-adrenergic receptors correlated with the affinity of each compound for the 3T3-L1 glucocorticoid receptor. Progesterone, which can bind to the glucocorticoid receptor but has only weak agonist activity, competitively inhibited the ability of dexamethasone to alter beta-adrenergic receptors. Protein synthesis, RNA synthesis, and N-linked glycosylation appeared to be necessary for the change in receptor subtype expression and the increase in beta-adrenergic receptor number induced by dexamethasone. The present study suggests that regulation of beta-adrenergic receptor expression in 3T3-L1 preadipocytes by dexamethasone is a glucocorticoid-specific effect which may require gene activation.
Mol Pharmacol 1987 Apr
PMID:Glucocorticoid regulation of beta-adrenergic receptors in 3T3-L1 preadipocytes. 303 66

To investigate the interaction of PRL and progesterone in regulating uterine gene expression, we have quantitated the concentration of PRL receptor and of uteroglobin (UG) mRNA in the endometrium of rabbits of different ages and after treatment with different hormones. During uterine differentiation in 2- to 4-week old rabbits, a marked increase in unoccupied uterine PRL receptor number was observed, presumably increasing uterine sensitivity to PRL. Receptor values for 4-week old rabbits were comparable to values for sexually mature, estrous females, but were lower than in 5-day pseudopregnant (PSP) animals. When total PRL receptor was determined by Scatchard analysis after in vitro desaturation with MgCl2, PSP animals again expressed the highest receptor concentration with no changes in the dissociation constant (Kd) values. To determine whether progesterone regulates uterine PRL receptor, long term ovariectomized rabbits (greater than 12 weeks) were treated with various combinations of hormones, and unoccupied and total uterine PRL receptors were determined. Progesterone treatment resulted in the highest concentration of both unoccupied and total PRL receptor after desaturation and removal of anti-ovine PRL antibodies with MgCl2. The value for total uterine PRL receptor was equivalent to the value for mammary gland, and the Kd values (2-4 x 10(-10) M) were similar. Treatment of long term ovariectomized rabbits with progesterone, with or without estradiol, produced an increase (P less than 0.05) in the UG mRNA content, which also occurred in PSP animals. PRL alone had no effect on UG mRNA but PRL plus progesterone increased (P less than 0.05) UG mRNA in a dose-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Endocrinol 1988 Dec
PMID:Servomechanism of prolactin and progesterone in regulating uterine gene expression. 321 59

We have examined the effects of estrogen and progestin agonist and antagonist ligands on regulation of progesterone receptor (PR) protein and mRNA levels in a variety of human breast cancer cell lines. By Northern blot analysis, using human PR cDNA probes, PR mRNA in T47D and MCF-7 cells appears as five species of approximately 11.4, 5.8, 5.3, 3.5, and 2.8 kilobases. PR mRNA species are not detected in the PR protein-negative breast cancer cell lines MDA-MB-231 and LY2. T47D cells contain high levels of PR mRNA and protein (detected by hormone binding assay or Western blot analysis), and the PR protein and mRNA content of T47D cells are reduced to about 10% of the control level within 48 h of treatment with 10 nM promegestone; 17, 21-dimethyl-19-nor-pregna-4,9-diene-3, 20-dione (R5020) or 16 alpha-ethyl-21-hydroxy-19-nor-pregn-4-ene-3,20-dione (ORG2058), both potent progestins. In contrast, treatment of T47D cells with the antiprogestin 17 beta-hydroxy-11 beta-[4-dimethylaminophenyl]-17 alpha-(1-propynyl)-estra- 4, 9-dien-3-one) (RU38486) reduces PR protein and mRNA levels only transiently. PR protein and mRNA are virtually undetectable in control MCF-7 cells grown in the absence of estrogens. When estradiol is administered to MCF-7 cells, the PR mRNA and protein levels increase gradually and proportionately (10- or 40-fold, respectively, in 3 days).(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Endocrinol 1988 Mar
PMID:Ligand-modulated regulation of progesterone receptor messenger ribonucleic acid and protein in human breast cancer cell lines. 339 53

The objective of the present study was to investigate the effect of cell density on hormonal responsiveness and lipoprotein utilization by cultured bovine luteal cells. Luteal cells obtained from regularly cycling dairy cows were plated at three culture densities: 0.5 X 10(6), 1 X 10(6) and 2 X 10(6) cells/flask in serum-free Ham's F-12 culture medium, and maintained for 9 days. Basal steroidogenesis was unaffected by cell density, while LH responsiveness was greatest in low density cultures. Progesterone produced in response to LH (10 ng/ml) was greater than control levels throughout the culture period in low density cultures. Luteal cells cultured at medium and high densities became responsive to LH only later in the culture period (days 5 and 9, respectively). In contrast, prostaglandin F2 alpha (PGF2 alpha, 100 ng/ml) was more effective in high density cultures, causing a complete inhibition of LH stimulation and returning progesterone levels to basal values. In low density cultures, treatment with PGF2 alpha + LH resulted in progesterone levels that were not significantly different from LH-treated cultures. There was no effect of cell density on utilization of either low density lipoprotein (LDL) or high density lipoprotein (HDL) for steroidogenesis. However, a synergistic effect of LH with either lipoprotein was observed in low and medium density, but not high density cultures. From these results, it is concluded that culture density can influence the responsiveness of bovine luteal cells to either LH or PGF2 alpha, but has no effect on lipoprotein utilization by these cells.
Mol Cell Endocrinol 1987 Oct
PMID:Cell density influences hormonal responsiveness but not lipoprotein utilization in cultured bovine luteal cells. 347 77

The kinetics of estrogen (E) modulation of retinol-binding protein (RBP) production in the liver of immature chicks were compared with those governing de novo induction of riboflavin carrier protein (RCP) in the same tissue. A single dose of E markedly enhanced the plasma levels of RBP without any detectable lag period to reach peak value by 24 h and this was followed by a decline to attain the baseline by 4 days. There was no amplification of the response during secondary stimulation unlike the case with RCP induction. With multiple E administration, the 4-fold increased plasma RBP concentrations were sustained at a steady state during both primary and secondary stimulations, whereas concomitant RCP concentration progressively increased with each hormone administration and this response was further amplified during secondary stimulation. Unlike RCP induction, enhanced RBP accumulation was not strictly E dose dependent although a minimal threshold level of the steroid was required to elicit measurable response. Progesterone (P) could neither modulate nor substitute for E in enhancing plasma levels of either of the 2 proteins while the anti-estrogens, en- and zuclomifene citrate severely suppressed the production of both the proteins. RCP induction was completely inhibited by both alpha-amanitin and cycloheximide for prolonged periods while E-stimulated RBP production was affected only partially by alpha-amanitin. Likewise, cycloheximide inhibition of RBP accumulation followed a pattern similar to that of hepatic general protein synthesis.
Mol Cell Endocrinol 1986 Jul
PMID:Estrogen modulation of retinol-binding protein in immature chicks: comparison with riboflavin carrier protein. 372 Oct 58

Ovariectomy or ovariohysterectomy on day 18 of pregnancy augmented mammary beta-casein content 28 h later. Progesterone injected immediately and 12 h after ovariectomy showed a clear inhibitory effect on casein synthesis. Estrogen induced a significant increase in mammary beta-casein content when injected 12 h after surgery. Treatment with CB-154 to prevent prolactin release did not affect the increase of casein induced by ovariectomy. When CB-154 was injected to ovariohysterectomized pregnant rats, significant reduction of casein synthesis was obtained. According to these findings, rat placental lactogen in the absence of prolactin and progesterone induces beta-casein synthesis. Therefore prolactin, ovarian and placental hormones interplay at the end of pregnancy for full expression of the mammary gland genome.
Mol Cell Endocrinol 1985 Feb
PMID:Hormonal regulation of casein synthesis at the end of pregnancy. 397 61

Progesterone-induced reinitiation of meiosis in Xenopus laevis oocytes involves a decrease in cAMP level. In these cells, adenylate cyclase is compartmentalized, with 25-30% in the plasma membrane fraction P-10000 (sedimenting at 10000 X g) and greater than 50% in the cytosol. Soluble adenylate cyclase appears not to be regulated via a GTP-binding regulatory protein (G/F) and is insensitive to progesterone. In contrast, membrane-bound adenylate cyclase seems to be linked to G/F, since it is stimulated by sodium fluoride, guanyl-5'-imidodiphosphate (Gpp(NH)p) and by cholera toxin; it is also inhibited by progesterone. The steroid inhibition is displayed towards basal and stimulated activities. The extent of progesterone inhibition of basal activity is dependent on Mg2+ and Mn2+ concentrations. The hormonal effect is independent of GTP concentration and is observed even in the presence of the non-hydrolysable analogue of GTP, Gpp(NH)p. The progesterone effect is not mediated by adenosine. Exposure of the P-10000 fraction to 5'-deoxy-5'-S-isobutylthioadenosine (a methyltransferase inhibitor) increases adenylate cyclase activity.
Mol Cell Endocrinol 1982 Oct
PMID:Adenylate cyclase in Xenopus laevis oocytes: characterization of the progesterone-sensitive, membrane-bound form. 629 Feb 96

Microinjection of cAMP-dependent protein kinase inhibitor (1.8 microM) increases the cAMP level of Xenopus oocyte. Its effect was observed in full-grown (stage VI) as well as in vitellogenic (stage IV) oocytes. In contrast the inhibitor I1 of protein phosphatase-1 blocks cAMP accumulation. Progesterone (1 microM) decreases the cAMP level in control and in PKI-treated oocytes of both stages. These results show that cAMP concentration is regulated by a cAMP-dependent phosphorylation indicating the presence of a feedback mechanism. The feedback control is disrupted when oocyte is induced to mature by progesterone.
Mol Cell Endocrinol 1983 Jul
PMID:cAMP-dependent protein kinase regulates in ovo cAMP level of the Xenopus oocyte: evidence for an intracellular feedback mechanism. 630 83

The mechanism by which progesterone modifies uterine smooth muscle cell contraction is still unknown. We investigated the biochemical basis of progesterone effects on myometrium of estradiol-primed rabbits. Progesterone did not affect adenylate cyclase basal activity and displayed no interaction with stimulators of myometrium adenylate cyclase (NaF, guanylyl nucleotides, beta-adrenoreceptor agonists, prostaglandins, forskolin) or with adenosine. On the other hand, adenosine inhibited myometrial adenylate cyclase, which correlates with its contracting properties in vivo; this inhibition is mediated through interaction at 'P sites'. We conclude that whilst adenosine inhibits myometrial adenylate cyclase by acting at 'P sites', progesterone does not interact directly with adenylate cyclase to regulate myometrial contractility.
Mol Cell Endocrinol 1984 May
PMID:The hormonal control of adenylate cyclase in rabbit myometrium: in vitro inhibition by adenosine and lack of effect of progesterone. 661 May 81


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