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PubMedDate not supplied

Estradiol increases susceptibility of goldfish to Trypanosoma danilewskyi.

We examined the in vivo and in vitro effects of estradiol on the host defense of goldfish against a hemoflagellate Trypanosoma danilewskyi. Estradiol (10(-6) M), significantly suppressed the mitogen-induced proliferation of peripheral blood lymphocytes in vitro. The parasitemia and mortality of goldfish implanted with tubing containing estradiol were significantly higher than that of sham operated control fish. In addition, the mitogen-induced proliferation of peripheral blood lymphocytes obtained from estradiol-implanted fish was significantly impaired when compared to that of lymphocytes obtained from untreated sham operated control fish. Estradiol implantation did not influence the ability of goldfish to resist a challenge infection with T. danilewskyi. These results indicate that estradiol can modulate the susceptibility to hemoflagellates by suppressing the host immune response.

Animals↗
PubMed1985

Synaptogenic effects of neonatal estradiol treatment in rat superior cervical ganglia.

Neonatal rats treated with testosterone propionate or 17-beta-estradiol during the first two postnatal weeks have more neurons and synapses in their superior cervical ganglia (SCGs) at 15 days of age than do vehicle-treated littermates. To determine whether a non-aromatizable androgen would similarly increase the number of SCG synapses, dihydrotestosterone (DHT) was injected into male rats beginning on the day of birth. The animals were sacrificed on postnatal day 15 and the SCGs removed on postnatal day 15. Counts of synapses showed no difference in the number of synapses between control and DHT-treated animals. These results suggest that the actions of testosterone to increase the numbers of SCG synapses may be via aromatization to estradiol. An additional study was done to determine whether the additional synapses formed in SCGs of animals treated with estradiol arise from neurons whose axons are in the cervical sympathetic trunk or from intrinsic neurons, i.e., SIF cells or other principal ganglion neurons. Neonatal males were injected with 17-beta-estradiol or vehicle beginning on the day of birth and continuing until the time of sacrifice on day 15. The number of intrinsic synapses formed under control and estradiol treatments was determined in SCGs of animals whose extrinsic synapses were caused to degenerate by severing the cervical sympathetic trunk bilaterally on postnatal day 13, two days before sacrifice. The total number of synapses (extrinsic plus intrinsic) in the ganglion after vehicle or estradiol treatment was determined in unoperated animals and used to calculate the number of extrinsic synapses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Stimulation of rat Schwann cell proliferation by estradiol: synergism between the estrogen and cAMP.

Schwann cells dissociated from sciatic nerves of 4- to 5-day-old rats were established in long-term primary cultures. After treatment with anti-Thy-1.1 and complement, pure Schwann cell cultures were obtained as confirmed by indirect immunofluorescence staining of the S-100 antigen. The effect of estradiol on Schwann cell proliferation was tested. The estrogen alone had no effect on cell multiplication, but in the presence of forskolin (5 microM) or dibutyryl cyclic AMP (dbcAMP, 1 microM), estradiol (100 nM) became a potent mitogen. This effect was specific since when the anti-estrogen ICI-164,384 (200 nM) was added to the cultures, it completely inhibited the mitogenic effect of estradiol. In the absence of the estrogen, ICI-164,384 did not inhibit dbcAMP-induced cell growth. The effect of progesterone was also tested in the presence of forskolin, and no influence on cell multiplication was seen. Specific and saturable binding sites for estradiol were measured in Schwann cells by whole cell assay after labeling cells at 37 degrees C with [3H]estradiol and about 3000 specific binding sites per cell were found. Treatment of the cultures with forskolin (5 microM) for 48 or 72 h, but not for shorter times, resulted in a two-fold increase in estradiol binding. Estrogen receptors were visualized inside Schwann cells with a monoclonal anti-ER antibody by indirect immunofluorescence staining. Double-label immunofluorescence of ER and S-100 showed that ER immunostaining was restricted to spindle-shaped Schwann cells expressing the S-100 antigen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Skeletal response of ovariectomized rats to low and high doses of 17 beta-estradiol.

Recent studies indicate that the mode of action of estrogen in preventing bone loss due to ovarian hormone deficiency may vary with the dose of the hormone. In this study four groups of ovariectomized animals were maintained on a wide range of doses of 17 beta-estradiol to further determine the relationship of dose to the mechanism by which estrogen prevents ovarian hormone deficiency bone loss. Ovariectomy caused a significant decrease in bone density and cancellous bone volume at the proximal metaphysis of the tibia. The decrease was prevented in a dose-dependent manner by estradiol. The rate of bone apposition in cancellous bone in the proximal tibia was increased by ovariectomy, and inhibited in a dose-dependent manner by estradiol. Similarly, ovariectomy increased the excretion of urinary hydroxyproline, an index of the rate of bone turnover, and serum alkaline and tartrate-resistant acid phosphatase. The increases were prevented in a dose-dependent manner by estradiol. In addition, the very high dose of estradiol, but not the lower doses, caused a marked (50%) decrease in serum osteocalcin. Our interpretation of these findings is that the low to very high doses of estradiol used in this study decreased the progression of the bone loss due to ovariectomy by suppression of the rate of bone turnover that involved the depression of both osteoclastic resorption and osteoblastic bone formation.

Animals↗
PubMed1988

Effect of estradiol on interleukin 1 synthesis by macrophages.

The effect of estradiol on interleukin 1 (IL-1) synthesis/secretion by rat peritoneal macrophages was investigated. Peritoneal adherent cells (PAC) from adult female rats secreted greater amounts of IL-1 spontaneously than those from age-matched male rats or prepubescent female rats. Ovariectomy led to reduced synthesis of IL-1 by PAC but estradiol replacement therapy of such rats effectively increased IL-1 synthesis. IL-1 secretion was also stimulated when PAC from male rats was incubated with estradiol. A combination of estradiol and LPS in vitro enhanced secretion of IL-1 by PAC even more than estradiol alone. These data provide new evidence suggesting that estradiol may play an important role in regulating synthesis of IL-1 by macrophages.

Aging↗
PubMedDate not supplied

Regulation of galanin secretion from pituitary cells in vitro by estradiol and GHRH.

The effects of estradiol and growth hormone-releasing hormone (GHRH) on galanin release from anterior pituitary cells were examined in vitro. 17-beta-Estradiol (0.001-10 nM) increased galanin secretion from anterior pituitary cells in a concentration-dependent manner. Estradiol (10 nM) increased galanin release 300 and 600% from pituitary cells of ovariectomized and male rats, respectively. Immunocytochemical studies demonstrated that estradiol (10 nM) increased the number of galanin-containing cells twofold after 4 days in culture. Growth hormone-releasing hormone (1 and 10 nM) increased and SRIF (1 and 10 nM) decreased galanin release from pituitary cells of ovariectomized and male rats. We conclude that estradiol increases galanin release by a direct effect on pituitary cells, in part by increasing the number of pituitary cells synthesizing galanin. In addition, GHRH stimulates galanin release when estradiol levels are low.

Animals↗
PubMed1985

Cytochemical demonstration of estrogen binding sites in breast cancer by estradiol covalently linked to horseradish peroxidase.

17 beta-Estradiol-6-carboxymethyloxime was covalently linked to horseradish peroxidase for the cytochemical demonstration of estrogen binding sites in breast cancer tissue. The affinity of the 17 beta-estradiol-horseradish peroxidase (E2-HRP) conjugate for the estrogen receptor in a human myometrial cytosol preparation was reduced by a factor of about 16 relative to that of 17 beta-estradiol. The estradiol concentration of the E2-HRP conjugate used in the incubations was in the range 2 X 10(-9) -1 X 10(-7) mol/l which, when the reduced affinity of the conjugate is taken into account, corresponds to 1 X 10(-10) -7 X 10(-9) mol/l unbound estradiol. The cytochemical reaction was carried out on cytofuge preparations of cell suspensions of breast cancer tissue. The intensity of the cytochemical reaction was microscopically evaluated by scoring. The results were analyzed in a plot allowing the calculation of an apparent score-max and an apparent Kd value. The reaction intensity was reduced to 20-25% of the control level by a 20-fold excess of 17 beta-estradiol. The cytochemical results correlated positively with the content of estrogen receptors in the cytosol as measured by a validated radioligand method.

Breast Neoplasms↗
PubMed1976

Site at which FSH regulates estradiol-17beta biosynthesis in Sertoli cell preparations in culture.

Sertoli cells were isolated from testes of 20-day-old rats and were maintained in primary culture. The ability of these cells to synthesise estradiol-17beta from a variety of exogenous substrates, progesterone, testosterone,androstenedione, 19-hydroxyandrostenedione and 19-hydroxytestosterone in the presence and absence of follicle-stimulating hormone (FSH) was examined. In the presence of each of the substrates alone for 24 h the rate of estradiol-17beta synthesis was very low. FSH (NIH-FSH-S11, 5 mug/ml) stimulated estradiol-17beta synthesis 75-fold when added to medium containing testosterone (5 X 10(-7)M) but caused only marginal stimulation when added to medium containing progesterone (5 X 10(-7) M). Both FSH and dibutyryl cyclic AMP (bu2cAMP) stimulated the conversion of each of the substrates, androstenedione, 19-hydroxyandrostenedione and 19-hydroxytestosterone to estradiol-17beta, and the effects were similar to those observed in the presence of testosterone. These data indicate that, under the culture conditions employed, progesterone is not an effective substrate for conversion to estradiol-17beta by Sertoli cells. Estradiol-17beta synthesis was stimulated by FSH in the presence of the C19 steluences the conversion of androgens to estrogens, either directly or indirectly, at the aromatisation step (i.e. the conversion of 19-hydroxylated androgens to estrogens).

Androstenedione↗
PubMedDate not supplied

High-affinity binding of the antiestrogen [3H]tamoxifen to the 8S estradiol receptor.

The interaction of tamoxifen (ICI 46,474), a synthetic antiestrogen, with uterine cytosol proteins of immature calf and rat has been studied directly using the tritiated compound labeled with a high specific activity. The binding complexes were measured by the dextrancoated charcoal, protamine sulfate and hydroxyapatite assays. Scatchard plots revealed a single class of high-affinity (KD congruent to 1.7 nM) binding sites, with a binding capacity similar to that of estradiol. Competitive experiments showed the same binding specificity for estrogens and antiestrogens. Sucrose gradient analysis revealed an 8S binding protein which could be partially proteolysed by trypsin into a 4S binding protein. Kinetic studies showed that the association rate of tamoxifen was 5 times lower than that of estradiol and reacted according to a second order kinetics. The first-order kinetics of dissociation was considerably higher than that of estradiol, giving a half-dissociation time of 20--40 min at 0--2 degrees C. In some cases tamoxifen displayed two slopes of dissociation, but the proportion of the slow-dissociating complex was always inferior to that found with estradiol. In contrast to estradiol, the kinetic constants ratio (k-/k+) gave a calculated dissociation constant, similar to that determined in equilibrium conditions (KD), agreeing with a simple reactional scheme. We conclude that the antiestrogen tamoxifen binds directly to the 8S cytosol receptor for estrogens and not to another receptor for the antagonists. In contrast to estradiol, the antagonist is rapidly dissociated from the receptor sites and is unable to protect them against thermal inactivation. The affinity of tamoxifen for its receptor sites as determined directly is surprisingly high when compared to its affinity evaluated indirectly by competitive experiments. It is then suggested that the two ligands either bind on two different sites of the same protein or induce a different conformational change of the same binding site.

Animals↗
PubMed1985

Estradiol increases the production of alpha 1-antichymotrypsin in MCF7 and T47D human breast cancer cell lines.

alpha 1-Antichymotrypsin (Achy) is an antiprotease of the acute inflammation phase, which is also released by MCF7 human breast cancer cells in culture. Using a fluorimetric assay with the synthetic substrate L-Seryl-L-Tyrosyl-2-N-naphthylamide, we have shown that a medium conditioned by MCF7 cells treated by estradiol inhibits the activity of alpha-chymotrypsin. This inhibition increased when physiological concentrations of estradiol were added to the cells for 2 days. It was due to an increased production of Achy and not to a direct effect of estradiol on alpha-chymotrypsin activity as shown by double immunoprecipitation with an antiserum against human alpha 1-antichymotrypsin. An increased accumulation by estradiol of an antigen located in the cytoplasm of MCF7 cells, which was revealed by immunoperoxidase staining with antibodies to Achy, also indicated that estradiol increased the production of Achy in these cells. Similar immunostaining was observed in a breast cancer tissue. Most of the estrogen regulated 60-68 kDa protein secreted by T47D cells (Chalbos et al. (1982) J. Clin. Endocrinol. Metab. 55, 276-283) was also specifically immunoprecipitated by the antibodies to Achy. Thus, alpha 1-antichymotrypsin is the first protein to be identified which is induced by estradiol and secreted by breast cancer cells.

Breast Neoplasms↗
PubMed1986

Induction of progestin receptors in the rat MtTF4 tumor of pituitary origin whose growth is inhibited by estradiol.

UNLABELLED: When the MtTF4 pituitary tumor was grown in male rats not treated by estradiol, the cytosol prepared from it contained very few binding sites for the synthetic [3H]ORG progestin. Following estradiol treatment there was a reversible increase of these binding sites. The ligand specificity and the sedimentation constant were shown to be similar to those of progestin receptors contained in other tissues. Daily treatment for 8 days with 10 micrograms 17 alpha-estradiol, 50 micrograms dihydrotestosterone or 50 micrograms dexamethasone did not induce progestin binding. IN CONCLUSION: (1) the virtual absence of progestin receptors in a tumor does not allow an absence of response to endocrine manipulation to be predicted; (2) the progestin receptors are induced by estradiol in the MtTF4 tumor despite the fact that the growth of this tumor is inhibited by estradiol; and (3) this work, taken together with previous reports, suggests that the estrogen receptors known to be located in the MtTF4 tumor have some functional properties in common with those tissues or cells whose growth is either stimulated by or insensitive to estradiol.

Animals↗
PubMed1989

Dependency of phorbol ester-induced gonadotropin secretion on estradiol.

Phorbol 12-myristate 13-acetate (PMA), which activates protein kinase C (PKC) was used to investigate the estradiol dependency of PKC-stimulated luteinizing hormone (LH) secretion from perifused anterior pituitaries. Infusions of PMA stimulated LH secretion from diestrous II, ovariectomized + estradiol-treated, and orchidectomized + estradiol-treated quartered pituitaries, by protein synthesis-dependent mechanisms. In contrast, pituitaries from intact, orchidectomized males, or ovariectomized females were unresponsive to PMA. Interestingly, dispersed male pituitary cells differed from male pituitary tissue blocks, in that the dispersed cells responded to PMA with increased LH secretion. These results indicate that PKC's ability to directly stimulate LH secretion is dependent on de novo protein synthesis and estradiol. Moreover, the effects of estradiol on PKC-stimulated secretion form at least one basis for the estradiol-induced increased responsiveness of gonadotrophs to GnRH. Additionally, it appears that dispersed pituitary cells may not respond to activators of PKC in a physiological manner.

Animals↗
PubMed1994

Estradiol inhibits growth hormone receptor gene expression in rabbit liver.

We studied the ontogeny of GH receptor mRNA levels and the effect of exogenous estradiol administration on GH receptor mRNA levels in rabbit liver. A solution hybridization-RNase protection assay revealed a predominant 370-base long protected band corresponding to the mRNA encoding the transmembrane GH receptor, and a 241-base long protected band, representing about 9.0%, with the predicted size for the truncated form of the GH receptor. To study the developmental profile of GH receptor expression, we studied 12 female rabbits, at ages 1, 3, 5 and 7 months. Maximal GH receptor mRNA levels were observed in 3-month-old animals and decreased in 7-month-old animals. To investigate the effect of estradiol, 8-week-old immature female rabbits were randomly divided into five groups, and received subcutaneous pellets containing either placebo or estradiol at doses of 0.1, 0.5, 1.5 and 5.0 mg for 3 weeks. Exogenous administration of estradiol, at doses that resulted in physiological circulating levels, induced a reduction in GH receptor expression, measured both by GH binding (36 and 46%), and GH receptor mRNA levels (38 and 87%), in animals receiving pellets containing 1.5 and 5.0 mg of estradiol, respectively. We conclude that estradiol decreases GH receptor expression in rabbit liver. The results of our study suggest that there is an inverse relationship between circulating estrogen concentrations and liver GH receptor expression.

Aging↗
PubMed1986

Estradiol target sites immunoreactive for beta-endorphin in the arcuate nucleus of rat and mouse hypothalamus.

Combined autoradiography and immunocytochemistry was performed to examine estradiol-concentrating neurons of the arcuate nucleus in the hypothalamus of ovariectomized rats and mice for beta-endorphin-like immunoreactivity. A high number of [3H]estradiol-labeled cells occurred in the arcuate nucleus of both species. Neurons immunoreactive for beta-endorphin could be visualized throughout the arcuate nucleus as well as ventrolaterally outside of this nucleus. Colocalization of [3H] estradiol nuclear labeling and beta-endorphin-like cytoplasmic immunoreactivity could be found scattered throughout the arcuate nucleus, most frequently in the ventromedial part, although most of the [3H]estradiol target neurons did not react with the antibodies. The results suggest that a subpopulation of beta-endorphin neurons is directly addressed by estradiol and that the arcuate nucleus contains different groups of estradiol receptive neurosecretory cells.

Animals↗
PubMed1992

Chronic estradiol treatment increases anterior pituitary but not striatal D2 dopamine receptor mRNA levels in rats.

The effect of chronic 17 beta-estradiol treatment (10 micrograms, twice each day, for 2 weeks) of ovariectomized rats on D2 dopamine (DA) receptor mRNA levels was investigated in striatum and anterior pituitary gland tissues. We used 32P-labeled probes specific for D2 receptor and beta-actin mRNAs in Northern blot analysis. The ratio of D2 DA receptor mRNA/beta-actin mRNA level was significantly increased in the anterior pituitary of estradiol-treated rats compared to vehicle-treated animals. The D2 DA receptor mRNA/beta-actin mRNA ratio in the striatum was not affected by estradiol treatment. However, the medial portion of the striatum showed a significantly lower ratio compared to the lateral portion of the striatum in both vehicle- and estradiol-treated rats. Thus, the estradiol effect on anterior pituitary D2 receptors may implicate transcriptional regulation, whereas our results do not support this hypothesis for the estradiol action on striatal D2 receptors.

Actins↗
PubMed1995

Noradrenergic vasorelaxation of porcine coronary arteries is enhanced by direct, acute exposure to 17 beta-estradiol.

1. We tested whether responses of isolated coronary arteries to adrenergic agents are altered by overnight (18-22 hr) or acute exposure to physiological levels of 17 beta-estradiol. 2. Sensitivity to relaxation by norepinephrine (-log M ED50) was enhanced significantly in isolated arteries after acute exposure to 10(-9) M 17 beta-estradiol. Neither alpha-adrenergic contraction to norepinephrine, nor beta-adrenergic relaxation to isoproterenol was affected by acute exposure to 17 beta-estradiol. 3. Responses of coronary arteries to relaxation or contraction by norepinephrine, as well as relaxation by isoproterenol, were not altered by overnight incubation with 17 beta-estradiol or by removal of the endothelium. 4. We conclude that relaxation of coronary arteries by norepinephrine is enhanced by acute, direct exposure to physiological levels of 17 beta-estradiol. This enhancement does not result from effects of estradiol to suppress alpha-adrenergic contraction to norepinephrine or increase coronary beta-adrenergic receptor sensitivity.

Animals↗
PubMed1996

Interaction of insulin-like growth factor-I and estradiol signaling pathways on hypothalamic neuronal differentiation.

Neurotrophic effects of estradiol and insulin-like growth factor-I were assessed in primary cultures from fetal rat hypothalamus. Cultured neurons were immunostained with an antibody for the microtubule-associated protein-2. While both estradiol and insulin-like growth factor-I increased the number of microtubule-associated protein-2-immunoreactive neurons and the extension of immunoreactive processes, the effect of these two factors was not additive. The estradiol-induced increases in neuronal numbers and extension of neuronal processes were blocked by either the estrogen receptor antagonist ICI 182,780 or by an anti-sense oligonucleotide to the estrogen receptor. Furthermore, incubation of the cultures with an anti-sense oligonucleotide directed against the insulin-like growth factor-I messenger RNA also blocked the effect of estradiol. In turn, the effects of insulin-like growth factor-I were blocked by the estrogen receptor antagonist ICI 182,780 and by the anti-sense oligonucleotide to the estrogen receptor. These findings suggest that estradiol-induced activation of the estrogen receptor in developing hypothalamic cells requires the presence of insulin-like growth factor-I, and that both estradiol and insulin-like growth factor-I use the estrogen receptor as a mediator of their trophic effects on hypothalamic neurons.

Animals↗
PubMed1988

Effects of estradiol on cerebral cortical neurons and their responses to adenosine.

The effects of iontophoretically applied 17 alpha- and 17 beta-estradiol on the spontaneous firing of, and actions of purines (adenosine, adenosine 5'-N-ethylcarboxamide) on, neurons in the rat cerebral cortex have been determined. Both steroids, applied as acetate, sulphate or hemisuccinate esters, depressed the spontaneous firing of approximately half of the neurons tested. 17 beta-Estradiol potentiated the inhibitory actions of adenosine on some neurons (26%) and antagonized the effects of adenosine on others (42%). 17 beta-Estradiol antagonized the inhibitory actions of adenosine 5'-N-ethylcarboxamide on 76% of the neurons tested, but did not enhance the actions of this uptake resistant adenosine analog. 17 alpha-Estradiol potentiated the actions of adenosine and adenosine 5'-N-ethylcarboxamide but failed to antagonize either purine. It is suggested that the potentiating effects of both stereoisomers on adenosine are a result of their ability to block adenosine uptake and that 17 beta-estradiol is also able to antagonize the actions of these purines. Antagonism of the effects of endogenously released adenosine may account for the excitant actions of 17 beta-estradiol on the central nervous system.

Adenosine↗