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At least 847 records · Page 47Linked to original sources
PubMed1982

Modulation of estrogen-induced peroxidase activity in the rat uterus by thyroid hormones.

The effect of thyroid hormones, iodide, propylthiouracil and other thyroid-active agents on estrogen receptor concentration and on the induction of peroxidase in the immature rat uterus by estradiol (E2) was examined T3 (0.5 mg/Kg) given daily for 6 days produced a large decrease in E2-induced uterine peroxidase but lowered only slightly the concentration of cytosolic or nuclear receptors in this organ. T4 also decreased the effect of E2 on uterine peroxidase induction and the inhibitory action of T3 was observed in thyroidectomized rats. The administration of iodide (10 mM) in the drinking water for 6 days caused a 2-fold increase in estrogen-induced peroxidase in both normal and thyroidectomized immature animals without influencing the estrogen receptor concentration in the uterus. The effect of other thyroid-active agents on serum T3 and T4 levels was also determined. Treatment for 6 days with propylthiouracil (6 mM) increased the concentration of estrogen receptors in the uterus and decreased serum T3 and T4 levels without any effect on uterine peroxidase activity while bromide and perchlorate did not influence these parameters. Possible mechanisms for the inhibitory effects of thyroid hormones on uterine peroxidase induction by E2 are discussed.

Animals↗
PubMed1983

Comparative studies of the 17 beta-estradiol receptors in rabbit liver, kidney and uterus.

The cytosol 17 beta-estradiol receptors from rabbit kidney, liver and uterus, compared under identical experimental conditions, were similar in terms of their pH-activity profiles, dependence on incubation temperature, sensitivity to sulfhydryl reagents and steroid specificity. 17 beta-[3H]-Estradiol binding was saturable with all three tissues, having an apparent dissociation constant of 4 X 10(-10)M. The binding of 17 beta-[3H]-estradiol in kidney, liver and uterus was inhibited by estrogens, including estrogen conjugates, but not by testosterone, progesterone or cortisol. The 17 beta-estradiol receptors of liver, kidney and uterus exhibited significant differences with respect to their chromatographic behaviour on heparin-Sepharose. Furthermore, a comparison of their sucrose density gradient centrifugation patterns showed that the 17 beta-[3H]-estradiol-receptor complex of liver and kidney sedimented at 3-4 S in both low and high ionic strength media, while the uterine receptor sedimented at 7-8 S in low ionic strength media and at 4-5 S in high ionic strength media. When the liver and uterine cytosol fractions were combined the uterine receptor was altered and sedimented at 3-4 S in low ionic strength media.

Animals↗
PubMed1984

Non-steroidal antioestrogens--receptor binding and biological response in rat uterus, rat mammary carcinoma and human breast cancer cells.

The non-steroidal antioestrogens tamoxifen, 4-hydroxytamoxifen, trioxifene, LY 117018 and LY 139481 have widely divergent affinities for oestrogen receptors from rat mammary tumours. The latter two compounds have much reduced partial agonist activity in rat uterus, compared to tamoxifen, but were less effective antitumour agents than tamoxifen. No direct correlation was established between receptor affinity and biological response in rat uterus or rat mammary carcinoma. However, in in vitro studies of growth inhibition of human breast cancer cells (MCF7), the order of potency was the same as the order of relative binding affinity. Differences in in vivo activity of these antioestrogens may be related to biological "half-life" which is dependent on the dose, route of administration and metabolic stability of the antioestrogens. Growth inhibition in MCF 7 cells did not correlate with affinity for tamoxifen-specific binding sites, nor was there any evidence for differences between antioestrogens in their mechanism of action on the rat uterus. It is concluded that the primary effects of antioestrogens are mediated by binding to oestrogen receptors.

Animals↗
PubMed1987

Effect of the antiprogestin RU-486 on progesterone inhibition of occupied nuclear estrogen receptor in the uterus.

The ability of the antiprogestin, RU-486, to reverse progesterone (P) antagonism of occupied nuclear E receptor retention was studied in the rat and hamster uterus. RU-486 was shown to effectively displace [3H]P binding from rat uterine cytosolic P receptor in in vitro competition assay. In contrast, no competition by RU-486 for [3H]P binding was observed for uterine cytosolic P receptor from the hamster uterus. In the presence of sustained serum levels (silastic implants) of P and estradiol (E), occupied nuclear E receptor was significantly inhibited in the rat uterus. At 6, 12 and 24h after RU-486 treatment (5 mg/animal, s.c.) uterine receptors for E and P were determined. No significant differences in cytosolic E and P receptors were observed between treated (E + P, + RU-486) and control (E + P alone) animals. However, by 6 h following RU-486 treatment, occupied nuclear E receptor retention increased significantly (0.30 +/- 0.05 vs 0.60 +/- 0.09, pmol/uterus) and reached a peak between 12 h (1.32 +/- 0.09) and 24 h (0.83 +/- 0.09). The increase in nuclear E receptor approached the level observed in animals with an E implant alone (1.55 +/- 0.15). Measurement of uterine fluid accumulation following RU-486 treatment showed an increase which paralleled that observed for occupied nuclear E receptor retention. A similar in vivo experiment in the hamster showed no reversal of P inhibition of occupied nuclear E receptor. These results show that: 1. RU-486 is an effective competitor for rat uterine P receptor but not hamster P receptor; 2. RU-486 can rapidly reverse P inhibition of uterine occupied nuclear E receptor in the presence of sustained serum levels of E and P; 3. The recovery of occupied nuclear E receptor is coincident with a resumption of E action (uterine fluid accumulation). The studies also provide a novel means by which antiprogestin activity can be assessed in vivo in the presence of sustained E and P serum levels, e.g. the reversal of P inhibition of uterine nuclear E receptor retention.

Animals↗
PubMed1988

Catechol estrogen formation in mouse uterus.

Estrogen 2/4-hydroxylase (ESH) and catechol-O-methyltransferase (COMT) activities in mouse liver and uterus were studied. While 2-hydroxyestradiol (2-OHE2) was the predominant product in the liver, equal amounts of 2- and 4-hydroxyestradiol were produced in the uterus. Two-hydroxyestradiol was the preferred substrate for COMT in both tissues, but the level of this enzyme activity was much less in the mouse uterus (17-fold less). Thus, preferential production of 4-hydroxyestradiol (4-OHE2) in the presence of relatively less deactivation provides a mechanism for the local formation of a more chemically active form of estrogen by uterine tissue.

Animals↗
PubMed1989

Size heterogeneity of affinity labeled estrogen receptors in the MtTF4 tumor whose growth is inhibited by estradiol, in pituitary gland and uterus.

UNLABELLED: Estrogen receptors (ER) of the MtTF4 tumor whose growth is inhibited by estradiol (E2) were analyzed and compared to those of tissues whose growth is stimulated by E2 (uterus and pituitary gland). Cytosol prepared in buffer containing protease inhibitors was incubated with [3H]tamoxifen aziridine ([3H]TAZ) in the presence or absence of non-radioactive competitor. The labeled proteins were precipitated, separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis in denaturing conditions and detected by fluorography. Two classes of ER were identified. The first class is of high molecular weight (Mr = 65,000-64,000). In normal tissues, it is indeed frequently made up of two subtypes as revealed by the presence of a doublet on autoradiograms. In the MtTF4 tumor these subtypes were only rarely suspected and never they were as marked and distinct as in normal tissues. The second class, of low molecular weight (Mr ! 54,000-52,000), is also frequently made up of two subtypes in the uterus and the proportion of this class is higher in the uterus of mature than of immature rats. The MtTF4 tumor contains this class of ER but, due to the presence of non-specifically labeled proteins in this region, its relative amount cannot be estimated and the doublet was exceptionally revealed. In the pituitary gland, this small receptor has not been found. CONCLUSIONS: (i) On the basis of molecular weight analyses, estrogen receptors are heterogeneous, (ii) the ER pattern depends on the type of tissue and the sexual maturity of rats but all the tissues examined contained at least one type of the "classic" high molecular weight receptor, and (iii) no evident correlation was found between the ER pattern and the positive or negative response to estradiol.

Animals↗
PubMed1989

Phenol red mimics biological actions of estradiol: enhancement of osteoblast proliferation in vitro and of type I collagen gene expression in bone and uterus of rats in vivo.

Since osteoblasts are direct targets for estradiol in vitro, and Phenol Red has been reported to bear estrogen-like bioactivity, we investigated whether the pH indicator also mimicked the biological effects of estradiol on bone cells in vitro. We then asked whether estrogenic effects of Phenol Red could be observed in vivo, firstly on the uterus, and if so, whether Phenol Red could also effect bone in vivo. The proliferation of calvarial osteoblasts was stimulated by commercially available preparations of Phenol Red in a dose-dependent manner at 1.5-50 microM. This effect was not abolished in the presence of an antibody against insulin-like growth factor I. In addition, Phenol Red increased alpha 1 (I) collagen mRNA levels of osteoblasts in vitro. 17 beta-estradiol (1.5 micrograms) or Phenol Red (10 mg) administration to immature female rats (45-50 g) resulted in a weight gain of the uterus, and alpha 1(I) procollagen transcripts were more abundant in RNA prepared from uterus of drug-treated rats than observed in the control rats. Similarly, higher procollagen mRNA steady-state levels were observed in RNA prepared from parietal bones of Phenol Red or estradiol-treated rats compared to RNA from control rats. The data extend previous findings in vitro by demonstrating that Phenol Red also exerts estrogen-like effects in vivo. Moreover, we show that Phenol Red stimulates bone cells and, therefore, is likely to interfere at least in experiments designed to investigate estrogen effects on osteoblasts.

Animals↗
PubMed1990

Catecholoestrogen synthesis and metabolism in the rabbit uterus during the periimplantation period.

Microsomal oestradiol-2/4-hydroxylase (OE-2/4-H) and cytosolic catechol-O-methyltransferase (COMT) (EC 2.1.1.6) activity in the uteri of pregnant and pseudopregnant rabbits during the periimplantation period were studied. The apparent Km for the 4-hydroxylation of oestradiol (3.18 microM) was considerably less than for the 2-hydroxylation reaction (13.36 microM), whereas the Vmax were almost equal. This suggests that 4-hydroxyoestradiol (4-OH-OE2) is the predominant product of OE-2/4-H in the rabbit uterus. These reactions were inhibited by SKF-525A, indicating the involvement of cytochrome P450 dependent monooxygenases. Uterine cytosolic COMT utilized 2-hydroxyestradiol (2-OH-OE2) as the preferred substrate as compared to 4-hydroxyoestradiol (4-OH-OE2). Since the rabbit uterus has a considerable capacity to synthesize 4-OH-OE2 and a lower capacity to metabolize it, it could be suggested that more 4-OH-OE2 than 2-OH-OE2 could be available to the uterus for its physiological activities. Furthermore, an increase in OE-2/4-H in Day 6 pseudopregnant and pregnant uteri with a concomitant decrease in COMT suggests the involvement of catecholoestrogens in the implantation process in the rabbit.

Animals↗
PubMed1990

Preferential nuclear binding of estrogen in the formalin-fixed rat uterus.

Rat uterus fixed overnight in buffered formalin retains the ability to specifically bind estradiol. However, the estrogen binding property of fixed tissue appears preferentially localized in the nuclear fraction regardless of hormonal status. Furthermore, the quantity of the nuclear estrogen receptor in fresh or fixed uterus is virtually identical in the presence or absence of estrogenic hormone. Yet, while both tissue preparations exhibit equivalent increases in the total nuclear receptor occupancy after hormone exposure, only the fresh uterus contains a major cytosolic estrogen binder which decreases in availability upon the estrogen-induced elevation of the nuclear bound steroid. However, the cytosolic estrogen receptor exhibits a significant loss in its ligand binding property after formalin exposure. Thus, the preferential localization of estrogen binding in the nuclear fraction of fixed whole tissue may just reflect that only the tightly bound nuclear estrogen receptor's functional and/or structural integrity survives long-term formation fixation. Our observation of estrogen binding in preserved tissue may also be a clinically useful tool in therapy analysis.

Animals↗
PubMed1992

The unicornuate uterus: clinical implications.

The unicornuate uterus is associated with a poor reproductive outcome and many gynecological problems. We collected data from 45 women with a unicornuate uterus. We found a high abortion rate of 22% in the first trimester and 16% in the second trimester. Premature labor occurred in 18%. The prevalence of infertility and endometriosis in women with a unicornuate uterus was comparable to women without the anomaly.

Abortion, Spontaneous↗
PubMed1994

Obstetrical prognosis of the septate uterus: a plea for treatment of the septum.

OBJECTIVE: To evaluate the obstetrical and perinatal implications of the septate uterus and assess the improvements of the prognosis after treatment of the septum. INVESTIGATION: This retrospective investigation was carried out in a single centre on 78 patients with septate uterus who had previously been correctly classified. A total of 203 pregnancies were observed. All complications occurring during the first, second and third trimesters and the neonatal outcome were logged. Furthermore, 25 patients in this sample underwent surgery which enabled reassessment of the obstetric and neonatal outcome. RESULTS: Prior to surgery, during the 203 pregnancies, the fetal loss rate during the first two trimesters was 47%, prematurity 17% and 89 children were alive, i.e. an overall perinatal mortality rate of 16.8% when pregnancy exceeded 24 weeks. After surgical treatment of the septum, the proportion of pregnancies proceeding subsequent to 24 weeks and infant survival changed, respectively, from 13.3% to 90% and from 4.4% to 87.5%. CONCLUSION: The obstetric and neonatal prognosis of septate uteruses is extremely unfavourable. This is radically transformed by treating the septum.

Female↗
PubMed1989

Effect of progestins, estradiol, and coenzymes NAD and NADPH on the interconversion of estradiol and estrone in rabbit uterus in vitro.

The biotransformation of estradiol (E2) and estrone (E1) in the uterus of rabbits treated with norgestrel (NG), norethindrone (NET), norethindrone acetate (NETA), progesterone (P4), and E2 either by subcutaneous injection in oil or by intrauterine steroid-releasing silastic implants was carried out under an in vitro short-term incubation system. The studies have shown that E2 stimulates 17 beta-hydroxysteroid dehydrogenase (17 beta-OHSD) much more than P4 as compared to untreated controls. The kinetic studies on E2 metabolism in the presence of added coenzyme NAD showed an initial rapid estrone formation and a gradual reconversion of E1 to E2. The addition of NADPH, ATP, and glucose-6-phosphate facilitates the reconversion of E1 to E2. The interconversion of E2 and estrone in the presence of coenzymes was five- to ten-fold higher in the endometrium than in the myometrium per milligram protein. Both E2 and progestins stimulate the uterine 17 beta-OHSD activity in rabbit uterus. This study further suggested that the hormone-induced metabolism of estradiol and estrone in the rabbit uterus is essentially modulated by the availability of coenzymes.

17-Hydroxysteroid Dehydrogenases↗
PubMed1977

The effects of ovariectomy and stretch on the regulatory profile and activity of the uterus.

Following ovariectomy of five New Zealand white rabbits at day 25 of pregnancy, the intrauterine pressure (IUP) and uterine progesterone (P) and prostaglandin (PG) levels were measured sequentially at days 25, 26 and 27. At day 25, when the uterine P and PGE and PGF were high, massive intrauterine treatment with 500 microng PGF2alpha provoked only a sustained contracture on which only low level oscillation in IUP was superimposed. At day 26, when the P levels had decreased significantly (P less than 0.001) and the PG levels had not changed significantly, 50 microng PGF2alpha significantly increased cyclic IUP as compared with the day 25 value (P less than 0.001). At day 27, when the P levels decreased further, as little as 5 microng PGF2alpha provoked still higher cyclic IUP, in spite of a significant reduction in PG levels (P less than o.05). Stretching the uterus of six post partum and six 26 days pregnant rabbits (after removing the uterine contents) significantly increased the uterine PGF levels (P less than o.001). However, stretch increased only cyclic IUP of the post partum uterus and was without effect on the pregnant uterus, which still had high P levels. These results indicate that the myometrium is activated by exogenous PG or stretch, regardless of whether the uterine PG levels increase, remain unchanged or even moderately decrease, provided that the uterine P levels are reduced to a critical value.

Animals↗
PubMed1982

Effect of corticosterone, hydrocortisone and prostaglandin fatty acid precursors on the spontaneous motility of the uterus isolated from ovariectomized rats.

The effect of corticosterone (CC, 0.4 and 1 microgram/ml) and of hydrocortisone (HC, 20 and 40 micrograms/ml) on the spontaneous motility and on prostaglandin (PG) generation in the uterus from ovariectomized rats, was studied. Both concentrations of CC depressed significantly the frequency of contractions but the isometric developed tension was affected only by the higher dose. HC significantly inhibited the isometric developed tension at both concentrations whereas the contractile frequency was only depressed by the higher one. The CC-inhibited motility was accompanied by a reduction in the amount of PGs released from the uterus into the bath solution. In addition, the influences of arachidonic acid (AA), linoleic acid (LA) and gamma-linolenic acid (alpha-LA) - 1 or 2 micrograms/ml - on the depression evoked by CC, were also explored. The fatty acids had no effect on the spontaneous uterine motility except in the case of alpha-LA at 1 microgram/ml. alpha-LA completely blocked the CC-evoked reduction of both tension and frequency; AA (1 microgram/ml) elicited a reversion only on frequency whereas LA had no effect at all. This reversion by a fatty acid PG-precursor might indicate that CC is able to diminish substrate availability for PG synthesis in the rat uterus.

Animals↗
PubMed1983

Prostaglandins in the uterus: modulation by steroid hormones.

Phospholipase A2 (PLA2), one of the enzymes considered to be rate-limiting in generating free arachidonic acid for prostaglandin (PG) synthesis, endogenous concentrations and in vitro production of PGs in the rat uterus were studied under various experimental conditions. Uterine PLA2 activity showed a 167-fold increase in ovariectomized rats bearing estradiol-17 beta (E2)-implants as compared to those treated with vehicle only. On the other hand, dexamethasone treatment reduced the E2-stimulable PLA2 activity by about 24-fold. The uterine PLA2 activity in the ovariectomized rat uterus was low and not altered by instillation of progesterone (P4) implants or by administration of dexamethasone. On the contrary, simultaneous placement of E2- and P4-implants prevented significantly the rise in PLA2 activity as observed under unopposed E2 exposure. Dexamethasone treatment further reduced the activity. The endogenous concentration of uterine PGF was several fold higher in the E2-implanted ovariectomized rats as compared to those without the E2-implants or carrying only P4-implants. The simultaneous treatment of the E2-implanted rats with P4 and/or dexamethasone reduced the uterine PGF concentrations considerably. The uterine PGF concentration was always lower in the ovariectomized rats under any condition if they were not treated with E2. Uterine PGE-A concentration did not change significantly between the ovariectomized rats and the ovariectomized rats carrying E2-implants. The treatment with P4 and/or dexamethasone, however, tended to decrease the PGE-A concentration. The production of PGF by the uterine homogenate increased by several fold in ovariectomized rats implanted with E2-silastic capsules as compared to those without the E2 implants. The treatments of the E2-implanted rats with P4 or dexamethasone did not alter this production. However, simultaneous exposure of E2-implanted rats to P4 and dexamethasone lowered the production rate of PGF in the uterus. The treatment of the ovariectomized rats with dexamethasone of P4 tended to elevate the uterine PGF production. The uterine PGE-A production followed more or less the same pattern. The analysis of our present data suggests that although a relationship exists between uterine PLA2 activity and PGF concentration, the role of PG synthetase could also be important in regulating PGF synthesis. Our study with dexamethasone, which showed inhibition of uterine PLA2 activity and decline in endogenous but not in vitro production of PGs, indicate that cellular integrity is essential for PLA2 to function as a rate-limiting step in PG synthesis.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Release of prostaglandins and leukotrienes from the rat uterus is an early estrogenic response.

The early estrogenic responses are considered to be involved in inducing embryo implantation in a progesterone (P4)-primed uterus. Because of their involvement in the process of implantation and decidualization, prostaglandins (PGs) and leukotrienes (LTs) could be the mediators of early estrogenic responses in a P4-primed uterus. Therefore, temporal effects of estrogen on the production and/or release of PGF2, PGF2 alpha, LTB4 and LTC4 by the P4-primed uterus of hypophysectomized rats were examined. Hypophysectomized mature female rats were injected for 4 days with P4 (2 mg/rat, s.c.) or with P4 plus a single injection of estradiol-17 beta (E2) (100 ng or 200 ng/rat, i.v.) on the last day of P4 treatment. In one set of experiments, animals were killed at 0.5, 2, 4, 8, 12 and 30th after the last steroid treatment. The production of PGs and Lts by uterine homogenates was measured by radioimmunoassays (RIAs). The production of PGE2 and PGF2 alpha in P4-treated animals showed peaks at 2, 6 and 12h. The superimposition of E2 on P4 treatment induced a higher production rate of PGE2 and PGF2 alpha at 0.5h and abolished the peaks induced by P4 at 2h, but not the peaks at 6 or 12h. Irrespective of the kind of steroid hormonal treatments, uterine production of LTs showed a rapid decline between 6 and 8h followed by a sharp rise at 12h. The superimposition of E2 on P4-treatment again increased the production rates of LTB4 and LTC4 at early hours, i.e. at 0.5 and 2h, respectively, as compared to P4 treatment only.

Animals↗
PubMed1993

Differential induction of c-jun expression by PGF2-alpha in rat ovary, uterus and adrenal.

The influence of PGF2 alpha on c-jun gene expression in ovary, uterus and adrenal was examined. Three and seven day postovulatory PMSG primed immature rats received 500 ug PGF2 alpha by two subcutaneous injections 8 hours apart. Control rats received saline. Animals were sacrificed 30 minutes after the second injection of PGF2 alpha. Tissues were obtained and frozen in liquid nitrogen. RNA extracted from ovary, uterus and adrenal was analyzed by Northern and slot blot. c-jun was expressed differentially in these organs. An increase in c-jun expression by PGF2 alpha treatment occurred in the ovary but not in the adrenal and uterus. The effect of PGF2 alpha on c-jun was stronger in older compared to younger corpora lutea. These results indicate differential regulation of c-jun by PGF2 alpha in steroidogenic and steroid responsive tissues and that c-jun might be linked to the mode of action of PGF2 alpha in luteolysis.

Adrenal Glands↗
PubMed1996

Differential expression of cyclooxygenase-1 and -2 proteins in rat uterus and cervix during the estrous cycle, pregnancy, labor and in myometrial cells.

The synthesis of prostaglandins in the uterus at term are modulated by two isoforms of the enzyme cyclooxygenase (COX): constitutive COX-1 and inducible COX-2. This study aims to characterize the expression of the protein for COX-1 and -2 in the rat uterus and cervix during the estrous cycle, pregnancy, and labor, and in cultured myometrial cells. Western immunoblotting of proteins was performed and quantitation of protein was obtained densitometrically. Results indicate: 1) the rat uteri, cervix, and isolated myometrial cells express both COX-1 and COX-2 proteins, 2) during pregnancy, both COX-1 and -2 increase, with a dramatic increase at parturition (250%-280%), 3) a 2-fold increase of cervical COX-2 is seen at spontaneous labor, 4) during proestrus and estrus, uterine expression of COX-2 is elevated, 5) both COX-1 and -2 were expressed by rat myometrial cells and treatment with IL-1 beta (10 ng/mL) produced a significant increase in COX-2, and 6) immunocytochemical studies show that both COX-1 and -2 were primarily localized to the epithelial cells of the endometrium and smooth muscle cells in the circular layers of the myometrium in the uterus and to the epithelial cells and smooth muscle cells in the cervix. Thus, we propose that increased expression of COX-2 may be involved at term in increased uterine contractility and cervical ripening.

Animals↗