Home About us Contact
|
Home About us Contact | ||
|
|
||
Oestrogen
Kinds of Oestrogen Terms modified by Oestrogen Selected AbstractsSTIMULATION OF OESTROGEN RECEPTOR-EXPRESSING ENDOTHELIAL CELLS WITH OESTROGEN REDUCES PROLIFERATION OF COCULTURED VASCULAR SMOOTH MUSCLE CELLSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2008Malin Odenlund SUMMARY 1Oestrogen reduces vascular smooth muscle cell proliferation in mouse vascular injury models. Data on the antiproliferative effect of oestrogen in cultured vascular smooth muscle cells (VSMC) are less conclusive than those obtained in whole animal studies. 2In the present study, we investigated the hypothesis that oestrogen-induced attenuation of VSMC proliferation is facilitated by the presence of endothelial cells (EC) using a coculture system of EC and VSMC. 3Treatment with a physiological concentration of oestrogen (17,-estradiol (E2); 100 nmol/L) had no effect on fetal calf serum (FCS)-stimulated DNA synthesis in either A7r5 VSMC or bEnd.3 EC. However, stimulation of bEnd. 3 cells with E2 in a coculture system of bEnd.3 and A7r5 cells reduced FCS-induced DNA synthesis in A7r5 cells by approximately 45%. The nitric oxide synthase inhibitor NG -nitro- l- arginine methyl ester (l -NAME; 100 µmol/L) did not reverse the oestrogen-induced attenuation of DNA synthesis. The antiproliferative effect of E2 may be mediated via either oestrogen receptor (ER) ,, ER, or both because the bEnd.3 cells expressed immunoreactivity for both ER subtypes. 4These data show that ER,- and ER,-expressing endothelial cells, which are stimulated with a physiological concentration of oestrogen, release a factor(s) that arrests the proliferation of cocultured VSMC. Oestrogen-induced attenuation of vascular smooth muscle cell proliferation is not prevented by l -NAME, suggesting that a mechanism other than endothelial NO is involved. [source] ROLE OF OESTROGEN IN THE CENTRAL REGULATION OF AUTONOMIC FUNCTIONCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2007TM Saleh SUMMARY 1In recent years, the role of oestrogen in women's health has been a subject of considerable scientific and popular debate. There is unquestionable evidence that oestrogen has both potent and long-lasting effects on several vital organ systems, including the cardiovascular system, the autonomic nervous system and, most recently, within the central nervous system itself. 2The research and medical community continues to debate whether the benefits of oestrogen therapy outweigh the risks in the treatment of the symptoms of menopause, the attenuation of the risk for cardiovascular insults, such as stroke and heart disease, and even the retardation of the progression of Alzheimer's disease. 3The recent evidence provided by the Heart and Estrogen/Progestin Replacement Study (HERS) II clinical trial suggesting that long-term exposure to combined oestrogen and progestin in post-menopausal women who have previously had a heart attack or stroke (for secondary prevention) may actually increase their risk of a subsequent cardiovascular insult has further fuelled the debate. However, there remain considerable gaps in our knowledge with respect to the actual mechanisms by which oestrogen exerts its various beneficial effects at the cellular level for the primary prevention of cardiovascular disease. This information is essential if we are to harness the positive aspects of oestrogen therapy in such a manner as to avoid or minimize the associated risks of increased oestrogen exposure in women who we know, with some certainty, to be at an increased risk of cancers of the uterus, cervix and breast tissue. [source] AGEING, OESTROGEN, PLATELETS AND THROMBOTIC RISKCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 8 2007Virginia M Miller SUMMARY 1Adverse thrombotic cardiovascular events increase in women coincident with the onset of menopause. 2Age past menopause may be an important variable in defining the benefit/risk of hormone treatments. 3Few studies have examined hormonal status as a variable of ageing using a polygenomic approach of both humoral and cellular components of the coagulation system. 4Longitudinal studies of a global set of platelet functions that define procoagulant activity (i.e. adhesion, aggregation, secretion and thrombin production) in individuals with documented hormonal status are needed to better understand how hormonal changes associated with ageing impact thrombotic risk. [source] OESTROGEN AND NIGROSTRIATAL DOPAMINERGIC NEURODEGENERATION: ANIMAL MODELS AND CLINICAL REPORTS OF PARKINSON'S DISEASECLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2007Bin Liu SUMMARY 1The exact nature of oestrogen (positive, negative or no effect) in the dopaminergic neurodegenerative disorder Parkinson's disease is controversial. 2In the present review, we summarize the data on oestrogen and nigrostriatal dopaminergic neurodegeneration in animal models and clinical reports of Parkinson's disease. 3Most animal studies support the ability of oestrogen to function as a neuroprotectant against neurotoxins that target the nigrostriatal dopaminergic system. 4Retrospective and prospective clinical studies generally support the findings from animal studies that oestrogen exerts a positive, or, at worst, no effect, in Parkinson's disease. 5Oestrogen was chosen as one of the 12 neuroprotective compounds to be attractive candidates for further clinical trials (Phase II or III) in 2003. [source] Oestrogen attenuates coronary vasoconstriction after angioplasty: role of endothelin-1EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2002T-M. Lee Abstract Background and aims There were controversies as to whether endothelin-1 is released after coronary angioplasty. We sought to determine whether endothelin-1 is released after coronary angioplasty and whether oestrogen administration can affect coronary vasomotor tone by reducing endothelin-1 concentrations. Methods The study was designed to prospectively investigate 24 consecutive patients scheduled for elective coronary angioplasty. Patients were randomized into two groups according to whether they did not (group 1, n = 12) or did (group 2, n = 12) have intracoronary treatment with oestrogen. Quantitative coronary angiography was monitored at baseline, immediately after successful angioplasty, and 15 min after the last deflation. Blood samples for measuring the levels of endothelin-1 were drawn from the ascending aorta and the coronary sinus simultaneously before angioplasty and 15 min after balloon dilatation. Results The diameters of the coronary artery at the dilated segments were significantly reduced 15 min after dilation compared with those immediately after dilation in group 1 from 3·20 ± 0·22 to 2·30 ± 0·23 mm (P < 0·001), respectively. The vasoconstriction was significantly blunted in group 2. The endothelin-1 levels from the coronary sinus rose significantly, by 29%, 15 min after angioplasty in group 1, which was attenuated after administering oestrogen. Significant correlation was found between the changes of coronary vasomotion of the dilated segment and endothelin-1 levels (r = 0·70, P = 0·01). Conclusion Endothelin-1 is released into the coronary circulation after angioplasty, and this vasoactive substance may contribute to the occurrence of vasoconstriction. The vasoconstriction is attenuated by oestrogen by reducing the endothelin-1 levels. This finding provided a new strategy to treat coronary vasoconstriction after angioplasty. [source] Effects of oestrogen agonists on human dermal fibroblasts in an in vitro wounding assayEXPERIMENTAL DERMATOLOGY, Issue 11 2009Susan Stevenson Abstract:, Oestrogen and dehydroepiandrosterone (DHEA) improve wound healing, but circulating levels decline significantly with age. Recently, the selective oestrogen receptor modulators (SERMs) tamoxifen and raloxifene have been shown to improve age-associated impaired wound healing. Therefore, we have evaluated the effects of 17,-oestradiol, ER, and ER, agonists, tamoxifen, raloxifene and DHEA on human dermal fibroblasts using an in vitro wound assay. An ER, agonist, 17,-oestradiol and DHEA all significantly accelerated cell migration; the DHEA effect was blocked with an aromatase inhibitor. Tamoxifen, raloxifene and DHEA all significantly increased DNA synthesis; the DHEA stimulatory effect was reversed by an aromatase inhibitor. This study demonstrates that 17,-oestradiol, an ER, agonist, tamoxifen, raloxifene and DHEA (following conversion to oestrogen) all have significant effects on human fibroblasts, the key mesenchymal cell involved in the wound healing process. Further understanding of the mechanisms involved may have important implications for the management of age-related impaired wound healing. [source] Determinants of within- and among-clutch variation in levels of maternal hormones in Black-Headed Gull eggsFUNCTIONAL ECOLOGY, Issue 3 2002Groothuis T. G. Summary 1.,Females of egg-laying vertebrates may adjust the development of their offspring to prevailing environmental conditions by regulating the deposition of hormones into their eggs. Within- and amng-clutch variation in levels of steroid hormones were studied in the egg yolks of the Black-Headed Gull (Larus ridibundus, Linnaeus) in relation to environmental conditions at the nest site. This species breeds in colonies of different densities and in different habitats, and the chicks hatch asynchronously. 2.,Egg yolks contained very high levels of androstenedione, substantial levels of testosterone and moderate levels of 5,-dihydrotestosterone. Oestrogen (17,-oestradiol) was not detected. 3.,Androgen levels increased strongly with laying order, irrespective of egg or yolk mass. This may compensate for the disadvantages of the later hatching chicks. These results have implications for adaptive hypotheses that were proposed for asynchronous incubation. 4.,Eggs of lighter clutches contained more androgens, perhaps to compensate for a lower nutritional quality of these eggs. 5.,Birds breeding in the periphery of a colony, being relatively more aggressive and having relatively large territories, laid eggs that contained more androgens than those of birds breeding in the centre. These high yolk androgen levels may facilitate growth and motor development of the chicks, which may be especially important for chicks developing at the periphery of a colony. Reduced levels may be adaptive for birds breeding in the centre, where risk of infectious diseases is high, since steroids may be immunosuppressive. 6.,Corrected for nest distance, clutches of birds in high vegetation, where predation risk is less severe and therefore competition for nest sites perhaps high, contained relatively high levels of androgens. It is suggested that the level of yolk androgens reflects the hormonal condition of the female, that in turn is influenced by her characteristics such as her age and aggressiveness, and the level of social stimulation. [source] Molecular mechanism of a cross-talk between oestrogen and growth factor signalling pathwaysGENES TO CELLS, Issue 8 2000Shigeaki Kato Oestrogen (E2) plays significant roles in variety of biological events such as the development and maintenance of female reproductive organs, bone and lipid metabolisms. More recently, from study of knock-out mice deficient in oestrogen receptor (ER) , and ER, it turned out that normal spermatogenesis requires the E2 actions. Furthermore, this female steroid hormone is also well known to be deeply involved in many pathophysiological events such as osteoporosis and cancer development in female reproductive organs. It is particularly well known that most breast cancer is dependent on E2 in its development. Such E2 actions are thought to be mediated through two subtypes of ERs. Growth factors have been shown to synergize in this E2 signalling pathway, although the actual molecular mechanism largely remains unknown. Recently, we found that the MAP kinase activated by growth factors phosphorylates the Ser118 residue of the human ER, A/B domain and this phosphorylation potentiates the N-terminal transactivation function (AF-1) of human ER,, indicating the possible molecular mechanism of a novel cross-talk between E2 and growth factor signalling pathways. More recently, we have identified a coactivator associating with the hER, AF-1 in a MAPK-mediated phosphorylation-dependent manner. In this review, the molecular mechanism of this cross-talk is discussed in terms of the transactivation function of ERs, and their coactivators. [source] Influence of oestrogen receptor , and , on the immune system in aged female miceIMMUNOLOGY, Issue 1 2003U. Islander Summary Oestrogen has a dichotomous effect on the immune system. T and B lymphopoiesis in thymus and bone marrow is suppressed, whereas antibody production is stimulated by oestrogen. In this study the importance of the oestrogen receptors (ER) ER-, and ER-, in the aged immune system was investigated in 18 months old-wild type (WT), ER-, (ERKO), ER-, (BERKO) and double ER-, and ER-, (DERKO) knock-out mice, and compared with 4 months old WT mice. Cell phenotypes in bone marrow, spleen and thymus, and the frequency of immunoglobulin (Ig) spot forming cells (SFC) were determined. We show here that the 17-,-oestradiol (E2)-induced downregulation of B lymphopoietic cells in bone marrow of young ovariectomized mice can be mediated through both ER-, and ER-,. However, only ER-, is required for the age-related increased frequency of immunoglobulin M (IgM) SFC in the bone marrow, as well as for the increased production of interleukin-10 (IL-10) from cultured splenocytes in aged mice. Furthermore, increased age in WT mice resulted in lower levels of both pro- and pre-B cells but increased frequency of IgM SFC in the bone marrow, as well as increased frequency of both IgM and IgA SFC in the spleen. Results from this study provide valuable information regarding the specific functions of ER-, and ER-, in the aged immune system. [source] Possible Role of Oestrogen in Pubertal Increase of Kiss1/Kisspeptin Expression in Discrete Hypothalamic Areas of Female RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2009K. Takase Kisspeptin, a peptide encoded by the Kiss1 gene, has been considered as a potential candidate for a factor triggering the onset of puberty, and its expression in the hypothalamus was found to increase during peripubertal period in rodent models. The present study aimed to clarify the oestrogenic regulation of peripubertal changes in Kiss1 mRNA expression in the anteroventral periventricular nucleus (AVPV) and hypothalamic arcuate nucleus (ARC), and to determine which population of kisspeptin neurones shows a change in kisspeptin expression parallel to that in luteinising hormone (LH) pulses at the peripubertal period. Quantitative reverse transcriptase-polymerase chain reaction and immunohistochemistry revealed an apparent increase in the ARC Kiss1 mRNA expression and kisspeptin immunoreactivity around the time of vaginal opening in intact female rats. The AVPV Kiss1 mRNA levels also increased at day 26, but decreased at day 31, and then increased at day 36/41. In ovariectomised (OVX) rats, ARC Kiss1 mRNA expression did not show peripubertal changes and was kept at a high level throughout peripubertal periods. Apparent LH pulses were found in these prepubertal OVX rats. Oestradiol replacement suppressed ARC Kiss1 mRNA expression in OVX prepubertal rats, but not in adults. Similarly, LH pulses were suppressed by oestradiol in the prepubertal period (days 21 and 26), but regular pulses were found in adulthood. The present study suggests that a pubertal increase of Kiss1/kisspeptin expression both in the ARC and AVPV is involved in the onset of puberty. These results also suggest that both LH pulses and ARC Kiss1 expression are more negatively regulated by oestrogen in prepubertal female rats compared to adult rats. [source] The Trophic Effects of Oestrogen on Male Rat Anterior Pituitary LactotrophsJOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2009L. A. Nolan Rapid but often transient changes in mitotic and apoptotic activity are important components of the pituitary response to changes in the hormonal environment. For example, bilateral adrenalectomy and orchidectomy each result in a wave of increased mitosis lasting approximately 1 week, mediated by the same population of trophically active and, to a large extent, endocrinologically inactive cells. By contrast to these tonic inhibitors of pituitary trophic activity, reports of a progressive increase in lactotroph numbers during pregnancy suggest that oestrogen is a potent and persistent pituitary mitogen. By comparing the amplitude and duration of male rat anterior pituitary mitotic responses to oestrogen treatment, to adrenalectomy, and to a combination of the two, the present study aimed to further clarify the characteristics of the oestrogen-induced trophic response, in particular whether lactotrophs are the predominant cell type involved. Adrenalectomy produced a wave of increased mitotic activity, which resolved within 7 days as expected, whereas oestrogen induced a significant increase in mitotic activity, which was sustained for the 14-day duration of the study. The trophic effects of combining adrenalectomy and oestrogen treatment were not additive in that the statistically insignificant upward trend in mitotic index during the first few days compared to oestrogen treatment alone was entirely abolished by oestrogen pre-treatment. The increase in mitotic activity in lactotrophs induced by oestrogen either with or without adrenalectomy did not result in an increase in the relative size of the prolactin-positive compared to prolactin-negative pituitary parenchymal cell numbers by the end of the study. Despite the marked increase in the lactotroph population that is reported during pregnancy, these data indicate that at least the early (i.e. within 2 weeks) mitotic response to pharmacological doses of oestrogen increases mitotic activity in the lactotroph subpopulation by only 5,8% relative to other cellular subpopulations. Unexpectedly, the mitotic response to oestrogen principally occurs in non-prolactin-containing cells and results in the recruitment, amongst other trophically responsive populations, of the entire subpopulation of prolactin-, adrenocorticotrophic hormone- and luteinising hormone-negative cells that respond mitotically to adrenalectomy. Oestrogen therefore has a previously unrecognised non-cell type-specific trophic effect in the pituitary that obscures the relative expansion of the lactotroph population by inducing concurrent increases in numbers of prolactin-negative cells, the nature of which at least in part remains to be determined. [source] Rapid Action of Oestrogen in Luteinising Hormone-Releasing Hormone Neurones: The Role of GPR30JOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2009E. Terasawa Previously, we have shown that 17,-oestradiol (E2) induces an increase in firing activity and modifies the pattern of intracellular calcium ([Ca2+]i) oscillations with a latency < 1 min in primate luteinising hormone-releasing hormone (LHRH) neurones. A recent study also indicates that E2, the nuclear membrane impermeable oestrogen, oestrogen-dendrimer conjugate, and the plasma membrane impermeable oestrogen, E2 -BSA conjugate, all similarly stimulated LHRH release within 10 min of exposure in primate LHRH neurones, indicating that the rapid action of E2 is caused by membrane signalling. The results from a series of studies further suggest that the rapid action of E2 in primate LHRH neurones appears to be mediated by GPR30. Although the oestrogen receptor antagonist, ICI 182, 780, neither blocked the E2 -induced LHRH release nor the E2 -induced changes in [Ca2+]i oscillations, E2 application to cells treated with pertussis toxin failed to result in these changes in primate LHRH neurones. Moreover, knockdown of GPR30 in primate LHRH neurones by transfection with human small interference RNA for GPR30 completely abrogated the E2 -induced changes in [Ca2+]i oscillations, whereas transfection with control siRNA did not. Finally, the GPR30 agonist, G1, resulted in changes in [Ca2+]i oscillations similar to those observed with E2. In this review, we discuss the possible role of G-protein coupled receptors in the rapid action of oestrogen in neuronal cells. [source] Oestrogen Regulates the Expression and Function of Dopamine Transporters in Astrocytes of the Nigrostriatal SystemJOURNAL OF NEUROENDOCRINOLOGY, Issue 9 2007S. Karakaya Dopamine is actively and specifically eliminated from the extracellular space by astrocytes and neurones through dopamine transporters (DAT) and, afterwards, either recycled into vesicles or metabolised. The availability of dopamine reflects a critical point in the regulation of dopamine activity within the nigrostriatal circuit under normal and pathological conditions. From previous studies, we know that oestrogen regulates the efficacy of dopaminergic neurones at the synaptic level and improves dopamine function during Parkinson's disease. Accordingly, we investigated the contribution of local astroglial for extracellular dopamine elimination and the impact of oestrogen on DAT expression and activity. Using neonatal striatal and midbrain astrocyte cultures, we could demonstrate that astrocytes possess a specific dopamine uptake machinery and express DAT at considerable levels. The application of 17,-oestradiol decreased the expression of DAT by 80% and 60% in midbrain and striatal astroglia cultures, respectively. The unspecific dopamine transporters (OCT3, VMAT2) were not detected in astroglia. Functionally, oestrogen exposure inhibited the clearance of dopamine from the extracellular space by 45% and 35% compared to controls in midbrain and striatal astroglia, respectively. The effect on DAT expression and activity was completely antagonised by the oestrogen receptor antagonist ICI 182 780. In conclusion, our data suggest that the positive reinforcement of dopamine transmission under physiological conditions and the alleviative impact of oestrogen under pathological conditions may be the result of a decline in DAT expression and therefore delayed dopamine uptake by astroglia. [source] Cells of the Arcuate Nucleus and Ventromedial Nucleus of the Ovariectomized Ewe that Respond to Oestrogen: A Study Using Fos ImmunohistochemistryJOURNAL OF NEUROENDOCRINOLOGY, Issue 11 2001I. J. Clarke Abstract Oestrogen produces a positive feedback effect on the secretion of gonadotropin releasing hormone (GnRH) and luteinizing hormone (LH) when implanted into the ventromedial/arcuate nucleus of the ovariectomized (OVX) ewe. This has led to the belief that it is in this area of the hypothalamus that oestrogen causes the preovulatory surge in GnRH/LH. To date, however, the cell types that are integral to this response have not been identified. The present study aimed to examine cellular responsiveness to oestrogen in this region of the brain using Fos immunohistochemistry and further aimed to determine the cell type that shows an acute response to oestrogen. OVX ewes (n = 4,6 per group) were given i.m. injections of oestradiol benzoate or oil (vehicle) and were killed 1,6 h later. Brains were perfused for immunohistochemistry. The number of cells in the arcuate nucleus which were immunopositive for Fos was greater (two- to fourfold) in the oestradiol benzoate-treated OVX ewes (n = 5) 1 h after injection. The number of Fos-positive cells in the ventromedial hypothalamic nucleus was 10-fold greater in the oestradiol benzoate-treated ewes 1 h after injection. Because there were high levels of Fos-immunoreactive cells in oil-treated ewes, we repeated the experiment with i.v. injection of 50 µg oestrogen or vehicle (n = 5). With this latter procedure, we found that oestrogen injection caused a significant increase in the number of Fos immunoreactive cells in the arcuate nucleus within 1 h, but there was no response in the ventromedial hypothalamus. To further characterize the types of cells that might respond to oestrogen, we double-labelled cells for Fos and either adrenocorticotropin hormone, neuropeptide Y or tyrosine hydroxylase (a marker for dopaminergic cells). These cell types could account for less than 30% of the total number of cells that were Fos-positive and oestrogen treatment did not cause an increase in the Fos labelling of any of these types of cell. These data show that oestrogen activates cells of the arcuate/ventromedial hypothalamus within 1 h of injection and that this response could relate to the feedback effects of this gonadal hormone. The majority of cells that produce Fos following oestrogen injection are of unknown phenotype. The data further suggest that induction of cells of the ventromedial hypothalamic nucleus require more prolonged oestrogen stimulus than cells of the arcuate nucelus. [source] Oestrogen Receptor ,-Immunoreactivity in Gonadotropin Releasing Hormone-Expressing Neurones: Regulation by OestrogenJOURNAL OF NEUROENDOCRINOLOGY, Issue 9 2001I. Kalló Abstract Double-label immunohistochemistry was employed to establish whether immunoreactivity for the , subtype of the oestrogen receptor (ER,-IR) is present in gonadotropin releasing hormone (GnRH)-containing cells. In the immortalized GnRH cell line, GT1-7, almost all nuclei were immunoreactive for ER,. In the preoptic area of ovariectomized rats, more than one-half of the GnRH neurones (52.0,63.5%) contained ER,-IR within the nucleus; a smaller proportion of these neurones (5,10%) displayed a particularly intense nuclear signal for ER,. The presence of ER,-IR in the nuclei of GT1-7 cells and GnRH neurones is consistent with recent reports of ER, mRNA in these cells. Oestrogen treatment reduced the percentage of GnRH neurones with detectable ER,-IR. The range of signal intensity for ER, and the incidence of the ER, signal in GnRH neurones were comparable following double-label immunohistochemistry involving either bright field or fluorescent techniques. These findings raise the possibility that ER, receptors mediate direct effects of oestrogen on GnRH neurones. [source] Comparison of Two Score Systems in Bcl-2 and Bax Protein Expression in Invasive Ductal Carcinoma of Breast and Relation with Oestrogen and Progestrone ReceptorsTHE BREAST JOURNAL, Issue 3 2009Ayatollahi Hossein MD No abstract is available for this article. [source] Rapid actions of oestrogen on gonadotropin-releasing hormone neurons; from fantasy to physiology?THE JOURNAL OF PHYSIOLOGY, Issue 21 2009Allan E. Herbison Oestradiol (E2) exerts critical homeostatic feedback effects upon gonadotropin-releasing hormone (GnRH) neurons to maintain fertility. In the female, E2 has both negative and positive feedback actions to suppress and stimulate GnRH neuron activity at different times of the ovarian cycle. This review summarizes reported rapid E2 effects on native embryonic and adult GnRH neurons and attempts to put them into a physiological perspective. Oestrogen has been shown to rapidly modulate multiple processes in embryonic and adult GnRH neurons including intracellular calcium levels, electrical activity and specific second messenger pathways, as well as GnRH secretion itself. Evaluation of in vivo data suggests that there is no essential role for rapid E2 actions in the positive feedback mechanism but that they may comprise part of the negative feedback pathway. Adult GnRH neurons are only likely to be exposed to E2 from the gonads via the circulation with appropriate physiological E2 concentrations in the rodent being 10,50 pm for negative feedback ranging up to 400 pm for positive feedback. Although most studies to date have examined the effects of supraphysiological E2 levels on GnRH neurons, there is accumulating evidence that rapid E2 actions may have a physiological role in suppressing GnRH neuron activity. [source] Uterine blood flow responses to ICI 182 780 in ovariectomized oestradiol-17,-treated, intact follicular and pregnant sheepTHE JOURNAL OF PHYSIOLOGY, Issue 1 2005Ronald R. Magness Oestrogen dramatically increases uterine blood flow (UBF) in ovariectomized (Ovx) ewes. Both the follicular phase and pregnancy are normal physiological states with elevated levels of circulating oestrogen. ICI 182 780 is a pure steroidal oestrogen receptor (ER) antagonist that blocks oestrogenic actions in oestrogen-responsive tissue. We hypothesized that an ER-mediated mechanism is responsible for in vivo rises in UBF in physiological states of high oestrogen. The purpose of the study was to examine the effect of an ER antagonist on exogenous and endogenous oestradiol-17, (E2,)-mediated elevations in UBF. Sheep were surgically instrumented with bilateral uterine artery blood flow transducers, and uterine and femoral artery catheters. Ovx animals (n= 8) were infused with vehicle (35% ethanol) or ICI 182 780 (0.1,3.0 ,g min,1) into one uterine artery for 10 min before and 50 min after E2, was given (1 ,g kg,1i.v. bolus) and UBF was recorded for an additional hour. Intact, cycling sheep were synchronized to the follicular phase using progesterone, prostaglandin F2,(PGF2,) and pregnant mare serum gonadotrophin (PMSG). When peri-ovulatory rises in UBF reached near peak levels, ICI 182 780 (1 or 2 ,g (ml uterine blood flow),1) was infused unilaterally (n= 4 sheep). Ewes in the last stages of pregnancy (late pregnant ewes) were also given ICI 182 780 (0.23,2.0 ,g (ml uterine blood flow),1; 60 min infusion) into one uterine artery (n= 8 sheep). In Ovx sheep, local infusion of ICI 182 780 did not alter systemic cardiovascular parameters, such as mean arterial blood pressure or heart rate; however, it maximally decreased ipsilateral, but not contralateral, UBF vasodilatory responses to exogenous E2, by ,55,60% (P < 0.01). In two models of elevated endogenous E2,, local ICI 182 780 infusion inhibited the elevated UBF seen in follicular phase and late pregnant ewes in a time-dependent manner by ,60% and 37%, respectively; ipsilateral , contralateral effects (P < 0.01). In late pregnant sheep ICI 182 780 also mildly and acutely (for 5,30 min) elevated mean arterial pressure and heart rate (P < 0.05). We conclude that exogenous E2,-induced increases in UBF in the Ovx animal and endogenous E2,-mediated elevations of UBF during the follicular phase and late pregnancy are partially mediated by ER-dependent mechanisms. [source] Immunohistochemical Localization of the Progesterone and Oestrogen , Receptors in the Uterine Horns of the African Giant Rat (Cricetomys gambianus)ANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 6 2009M.-C. Madekurozwa Summary The present study investigated the immunolocalization of the progesterone and oestrogen , receptors in the uterine horns of the African giant rat during the oestrous cycle. The progesterone and oestrogen , receptors were demonstrated in various cellular constituents of the endometrium, myometrium and perimetrium. The intensity of progesterone and oestrogen , receptor immunostaining in the endometrial and myometrial layers of the uterine horns varied during the oestrous cycle. The intensity of oestrogen , receptor immunoreactivity in the luminal epithelium was high during pro-oestrus, oestrus and dioestrus. Progesterone and oestrogen , receptor immunoreactivity in the endometrial epithelia was absent during metoestrus. Moderate to strong immunostaining for the progesterone and oestrogen , receptors was demonstrated in the myometrial smooth muscle cells during pro-oestrus, oestrus and dioestrus. The intensity of progesterone and oestrogen , receptor immunostaining in the myometrial smooth muscle cells was low during metoestrus. Stromal cells in the perimetrium consistently expressed progesterone and oestrogen , receptor immunoreactivity throughout the oestrous cycle. The findings of the study indicate that in the giant rat the immunolocalization of the progesterone and oestrogen , receptors, in endometrial and myometrial regions of the uterine horns, varies during the oestrous cycle. [source] Oestrogen and progesterone receptors in primary mucinous carcinoma of skinAUSTRALASIAN JOURNAL OF DERMATOLOGY, Issue 4 2005Kanwardeep S Kwatra SUMMARY A 74-year-old man presented with a recurrent indolent growth in the left axilla. Fine-needle aspiration cytology and histopathological examination showed a picture of mucinous adenocarcinoma. Clinical examination and systemic investigations failed to detect any primary lesion elsewhere and hence, a diagnosis of primary mucinous carcinoma of the skin was made. This tumour shows histological resemblance to mucinous carcinoma of breast. We also demonstrated expression of oestrogen and progesterone receptors in this tumour. This observation suggests that there is a potential of using antioestrogenic therapy in patients with primary cutaneous mucinous carcinoma, especially because of its high rate of local recurrence. [source] How Oestrogen or Progesterone might Change a woman's susceptibility to HIV-1 infectionAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 5 2002Li Mingjia ABSTRACT Worldwide, 18.5 million women are infected with the human immunodeficiency virus (HIV-1). At least 80% of these HIV infections have occurred as a result of sexual intercourse with an infected male partner. This review focuses on how HIV-1 enters the human female reproductive tract, and how oestrogen or progesterone, by altering the cervicovaginal epithelium, might change a woman's susceptibility to HIV infection. Experiments on hysterectomised Rhesus monkeys suggest that the vagina, rather than the cervix or uterus, is the main site of viral entry. If ovariectomised monkeys are given systemic oestrogen treatment, this makes them completely resistant to infection by intravaginally administered simian immunodeficiency virus (SIV), whereas progesteronetreated animals, like the untreated controls, are extremely susceptible. Some studies have also shown that women on systemic long-acting gestagen-only contraceptives have a thinner vaginal epithelium and hence might be more susceptible to HIV infection; this is certainly true of post-menopausal women. The beneficial effects of oestrogen are thought to be due to increased thickness and cornification of the cervicovaginal epithelium, which prevents the virus from coming into contact with the target Langerhans cells (LCs). Topical vaginal oestrogen treatment is widely used as a safe and effective way of thickening and keratinising the vaginal epithelium in post-menopausal women. Perhaps this could be an exciting new way of protecting women from HIV infection. [source] Oestrogen Promotes Coronary Angiogenesis even under Normoxic ConditionsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2008Mehdi Nematbakhsh Oestrogen has angiogenic properties under hypoxic condition, and if oestrogen also induces angiogenesis under normoxic condition, it could be used in combination with other angiogenic therapies in the treatment of ischaemic heart disease. In this study, we evaluated the angiogenic effect of high-dose oestrogen treatment in normoxic rat heart tissue. Fifty-two ovariectomized rats were randomized in oestrogen-treated and control groups. 17,-Oestradiol (1 mg/week) and normal saline (1 mg/week) were administered intramuscularly in the treatment and control groups for 2 months. After that, coronary capillary density and coronary vessel permeability were measured. The serum vascular endothelial growth factor (VEGF) level was also measured before and after the treatment. The results indicate that coronary capillary density (number of capillary per square millimetre) and coronary vessel permeability (fluorescence intensity) were significantly higher in the oestrogen-treated group than in the control group (628 ± 26 per mm2 versus 540 ± 26 per mm2; P < 0.05 and 207 ± 10 versus 147 ± 19 per gram tissue; P < 0.05). Oestrogen treatment increased serum VEGF level in the oestrogen-treated group compared to the control group (52 ± 3 versus 33 ± 6 pg/ml; P < 0.05), but interestingly VEGF was also increased in the control group after placebo treatment. It seems that high-dose oestrogen administration has angiogenic properties even in normoxic conditions. These angiogenic properties may result from oestrogen's direct effect on VEGF or other mechanisms, such as endothelial progenitor cell mobilization. Because of the broad effect of oestrogen on angiogenic growth factors and endothelial cells, more studies are required to clarify angiogenic properties of high-dose oestrogen. [source] Early structural effects of oestrogen on pudendal nerve regeneration in the ratBJU INTERNATIONAL, Issue 6 2004D.D. Kane OBJECTIVE To determine the early effects of oestrogen on the ultrastructure of the pudendal nerve and distal nerve fascicles near the external urethra sphincter (EUS) after a pudendal nerve crush injury. The pudendal nerve is one of the pelvic floor tissues injured during vaginal delivery, possibly contributing to the development of stress urinary incontinence (SUI) in women, the symptoms of which often do not appear until menopause, implicating hormonal factors. MATERIALS AND METHODS Twenty-seven virgin female Sprague-Dawley rats were anaesthetized and underwent ovariectomy. Three days later, they had one of four procedures: bilateral pudendal nerve crush plus implant of a subcutaneous oestrogen-containing capsule (NC+E); nerve crush plus implant of a sham saline-containing capsule (NC+S); no nerve crush with an oestrogen capsule; or no nerve crush with a sham capsule. After 2 weeks the pudendal nerves and urethral tissues were prepared for light and electron microscopy. The number of axons, myelin figures and endoneurial nuclei in the pudendal nerve segment distal to the lesion were counted. Nerve fascicles near the EUS were also counted and categorized as normal or showing signs of degeneration and/or regeneration. The location of each nerve fascicle was specified as either ventral or dorsal. RESULTS As there were no significant differences between the two control groups they were combined to form a single control group. In the distal pudendal nerve there were significantly fewer myelinated axons and large myelinated axons in the NC+E and NC+S groups than in the control group. There were three times as many large unmyelinated axons in the NC+E group than in either the NC+S or control groups (P < 0.05). There were only half as many nerve fascicles near the ventral side of the EUS in the NC+S group than in both the control and NC+E groups (P < 0.05). CONCLUSION Oestrogen appears to affect large unmyelinated axons in both the injured pudendal nerve and at the denervated EUS target. After pudendal nerve crush, nerve fascicles with evidence of degeneration or regeneration near the EUS appear to be spared with oestrogen treatment, particularly in the ventral region. These observations may reflect the early stages of a neuroregenerative effect of oestrogen. Additional studies are needed to confirm these results at later periods and with functional methods. [source] Mitogenic effects of oestrogen mediated by a non-genomic receptor in human colonBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 12 2000Mr D. C. Winter Background Oestrogens are important mitogens in epithelial cancers, particularly where tumours express complementary receptors. While the traditional model of oestrogen action involves gene-directed (genomic) protein synthesis, it has been established that more rapid, non-genomic steroid hormone actions exist. This study investigated the hypothesis that oestrogen rapidly alters cell membrane activity, intracellular pH and nuclear kinetics in a mitogenic fashion. Methods Crypts isolated from human distal colon and colorectal cancer cell lines were used as robust models. DNA replication and intracellular pH were measured by radiolabelled thymidine incorporation (12 h) and spectrofluorescence imaging respectively. Genomic protein synthesis, sodium,hydrogen exchanger (NHE) and protein kinase C (PKC) activity were inhibited with cycloheximide, ethylisopropylamiloride and chelerythrine chloride respectively. Results Oestrogen induced a rapid (less than 5 min) cellular alkalinization of crypts and cancer cells that was sensitive to NHE blockade (P < 0·01) or PKC inhibition (P < 0·01). Oestrogen increased thymidine incorporation by 44 per cent in crypts and by up to 38 per cent in cancer cells (P < 0·01), and this was similarly reduced by inhibiting the NHE (P < 0·01) or PKC (P < 0·05). Conclusion Oestrogen rapidly activates cell membrane and nuclear kinetics by a non-genomic mechanism mediated by PKC but not gene-directed protein synthesis. © 2000 British Journal of Surgery Society Ltd [source] Modulation of growth hormone action by sex steroidsCLINICAL ENDOCRINOLOGY, Issue 4 2006Udo J. Meinhardt Summary Growth hormone (GH) is a major regulator of growth, somatic development and body composition. Sex steroids can act centrally by regulating GH secretion and peripherally modulating GH responsiveness. This review addresses data of potential clinical relevance on how sex steroids modulate GH secretion and action, aiming to increase the understanding of sex steroid/GH interactions and leading to improved management of patients. Sex steroids regulate GH secretion directly as well as indirectly through IGF-I modulation. Testosterone stimulates GH secretion centrally, an effect dependent on prior aromatization to oestrogen. Oestrogen stimulates GH secretion indirectly by reducing IGF-I feedback inhibition. Whether oestrogen stimulates GH secretion centrally in females is unresolved. Gonadal steroids modify the metabolic effects of GH. Testosterone amplifies GH stimulation of IGF-I, sodium retention, substrate metabolism and protein anabolism while exhibiting similar but independent actions of its own. Oestrogen attenuates GH action by inhibiting GH-regulated endocrine function of the liver. This is a concentration-dependent phenomenon that arises invariably from oral administration of therapeutic doses of oestrogen, an effect that can be avoided by using a parenteral route. This strong modulatory effect of gonadal steroids on GH responsiveness provides insights into the biological basis of sexual dimorphism in growth, development and body composition and practical information for the clinical endocrinologist. It calls for an appraisal of the diagnostic criteria for GH deficiency of GH stimulation tests, which currently are based on arbitrary cut-offs that do not take into account the shifting baseline from the changing gonadal steroid milieu. In the management of GH deficiency in the hypopituitary female, oestrogen should be administered by a nonoral route. In hypopituitary men, androgens should be replaced concurrently to maximize the benefits of GH. In the general population, the metabolic consequences of long-term treatment of women with oral oestrogen compounds, including selective oestrogen receptor modulators, are largely unknown and warrant study. [source] Oestrogen receptor-alpha activation augments post-exercise myoblast proliferationACTA PHYSIOLOGICA, Issue 1 2010A. Thomas Abstract Aim:, Our laboratory has shown that oestrogen acts to augment myoblast (satellite cell) activation, proliferation and total number and that this may occur through an oestrogen receptor (OR)-mediated mechanism. The purpose of this study was to further investigate the mechanism of oestrogen influence on augmentation of post-exercise myoblast numbers through use of a specific OR-, agonist, propyl pyrazole triol (PPT). Methods:, Ovariectomized rats were used (n = 64) and separated into four groups: sham, oestrogen supplemented, agonist supplemented, and a combined oestrogen and agonist supplemented group. These groups were further subdivided into control (unexercised) and exercise groups. Surgical removal of white vastus and soleus muscles was performed 72 h post-exercise. Muscle samples were immunostained for the myoblast markers Pax7 and MyoD. Results:, A significant increase in total (Pax7-positive) and activated (MyoD-positive) myoblasts was found in all groups post-exercise. A further significant augmentation of total and activated myoblasts occurred in oestrogen supplemented, agonist supplemented and the combined oestrogen and agonist supplemented groups post-exercise in white vastus and soleus muscles relative to unsupplemented animals. Conclusion:, These results demonstrate that both oestrogen and the specific OR-, receptor agonist, PPT, can significantly and to similar degrees augment myoblast number and activation following exercise-induced muscle damage. This suggests that oestrogen acts through an OR-mediated mechanism to stimulate myoblast proliferation following exercise, with OR-, playing a primary role. [source] Hormone receptor status in breast cancer , a comparison between surgical specimens and fine needle aspiration biopsiesCYTOPATHOLOGY, Issue 3 2003L. Löfgren The present study was performed to evaluate the immunocytochemical analysis (ICA) of oestrogen (ER) and progesterone receptor (PR) in fine needle aspiration (FNA) biopsies from primary breast cancers as compared with the established enzyme immunoassays (ER-EIA and PR-EIA) based on cytosol homogenates from the corresponding resected tumour specimens. A total of 967 primary breast cancers were assessed for ER and PR content by both methods. Correlations between EIA and ICA expressed as percentage of tumour cells with a positive staining were highly significant (P < 0.001) for ER and PR. Staining intensity yielded only limited additional information. The concordance between the two techniques was about 80%. Evaluation of biological parameters by FNA may be useful to decide the optimal treatment for breast cancer patients. [source] Oestradiol replacement treatment and glucose homeostasis in two men with congenital aromatase deficiency: evidence for a role of oestradiol and sex steroids imbalance on insulin sensitivity in menDIABETIC MEDICINE, Issue 12 2007V. Rochira Abstract Aims The role of sex steroids in glucose and insulin metabolism in men remains unclear. To investigate the effects of sex steroids and oestrogen on insulin sensitivity in men, we studied two male adults with aromatase deficiency (subject 1 and subject 2). Methods The effects of transdermal oestradiol (tE2) treatment at different dosages on insulin sensitivity were studied before tE2 treatment (phase 1), and after 6 months (phase 2) and 12 months of tE2 treatment (phase 3) by means of homeostasis model assessment,insulin resistance (HOMA-IR) and Quantitative Insulin Sensitivity Check Index (QUICKI), insulin tolerance test (ITT), and oral glucose tolerance test (OGTT). The latter was performed only in subject 1, as subject 2 suffered from Type 2 diabetes. Results The restoration of normal serum oestradiol led to improved insulin sensitivity, as shown by changes in HOMA-IR and QUICKI. The ITT provided evidence of improved insulin sensitivity during tE2 treatment. Insulin secretion after OGTT was reduced during tE2 treatment in subject 1. After 12 months of tE2 treatment, insulin sensitivity was improved compared with in phases 1 and 2. Conclusions The study suggests a direct involvement of oestrogens in insulin sensitivity, and supports a possible role of oestradiol : testosterone ratio, which may be as influencial as the separate actions of each sex steroid on glucose homeostasis. [source] Post natal oestrogen administration stimulates precocious endometrial gland development in the horseEQUINE VETERINARY JOURNAL, Issue 7 2009S. WILSHER Summary Reasons for performing study: Fillies completely devoid of endometrial glands (uterine gland knockout; UGKO) would make ideal experimental models in which to study the role of endometrial histotroph in embryogenesis and early fetal development in the mare. Hypothesis: Administration of a synthetic progestagen plus oestrogen to newborn filly foals and, thereafter, at regular intervals to age 6 months, would permanently suppress endometrial gland development. Methods: Nine half-sister Thoroughbred filly foals were treated, in 3 groups, with: A) the weakly active progestagen, norgestomet, administered from birth to age 6 months, in subcutaneous implant form plus oestradiol valerate and norgestomet i.m. at fortnightly intervals; B) the strongly active oral progestagen, altrenogest, administered daily from birth to age 6 months plus fortnightly injections of oestradiol valerate and norgestomet; C) nothing (untreated controls). Endometrial biopsies were recovered from all fillies at ages 6 months and 2 years to assess the degree of endometrial gland morphogenesis and to determine immunohistochemically the presence or absence of oestrogen and progesterone receptors in the endometrial tissues. Results: Groups B and C showed no endometrial gland development, whereas Group A fillies showed a high degree of endometrial gland development, plus strong staining for both oestrogen and progesterone receptors at age 6 months. All 9 fillies showed full normal endometrial gland morphogenesis, development and function at age 2 years. Conclusions and relevance: While the administration of a strongly active progestagen over-rode the actions of the concomitantly administered oestrogen and suppressed endometrial gland development during the period of administration, treatment with oestradiol valerate together with a weakly active progestagen, stimulated precocious endometrial gland development. Neither steroid was able to create the desired UGKO experimental model and all fillies showed normal endometrial gland development and fertility after puberty. Hence, ovarian oestrogen, not progesterone, appears to be the basic stimulus for endometrial gland morphogenesis in the horse. [source] Oestrogen attenuates coronary vasoconstriction after angioplasty: role of endothelin-1EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2002T-M. Lee Abstract Background and aims There were controversies as to whether endothelin-1 is released after coronary angioplasty. We sought to determine whether endothelin-1 is released after coronary angioplasty and whether oestrogen administration can affect coronary vasomotor tone by reducing endothelin-1 concentrations. Methods The study was designed to prospectively investigate 24 consecutive patients scheduled for elective coronary angioplasty. Patients were randomized into two groups according to whether they did not (group 1, n = 12) or did (group 2, n = 12) have intracoronary treatment with oestrogen. Quantitative coronary angiography was monitored at baseline, immediately after successful angioplasty, and 15 min after the last deflation. Blood samples for measuring the levels of endothelin-1 were drawn from the ascending aorta and the coronary sinus simultaneously before angioplasty and 15 min after balloon dilatation. Results The diameters of the coronary artery at the dilated segments were significantly reduced 15 min after dilation compared with those immediately after dilation in group 1 from 3·20 ± 0·22 to 2·30 ± 0·23 mm (P < 0·001), respectively. The vasoconstriction was significantly blunted in group 2. The endothelin-1 levels from the coronary sinus rose significantly, by 29%, 15 min after angioplasty in group 1, which was attenuated after administering oestrogen. Significant correlation was found between the changes of coronary vasomotion of the dilated segment and endothelin-1 levels (r = 0·70, P = 0·01). Conclusion Endothelin-1 is released into the coronary circulation after angioplasty, and this vasoactive substance may contribute to the occurrence of vasoconstriction. The vasoconstriction is attenuated by oestrogen by reducing the endothelin-1 levels. This finding provided a new strategy to treat coronary vasoconstriction after angioplasty. [source] | ||||||||||||||||||||||||||||||||||||||||