Oestrogen Treatment (oestrogen + treatment)

Distribution by Scientific Domains


Selected Abstracts


Regulation and Expression of Progesterone Receptor mRNA Isoforms A and B in the Male and Female Rat Hypothalamus and Pituitary Following Oestrogen Treatment

JOURNAL OF NEUROENDOCRINOLOGY, Issue 3 2002
R. E. M. Scott
Abstract Progesterone receptors play a central role in neuroendocrine and behavioural regulation. To gain insight into the sex- and tissue-specific regulation of progesterone receptors, protein binding on a progesterone receptor-oestrogen response element and mRNA levels for progesterone receptor (PR)-A and PR-B were compared between female and male rats following oestradiol benzoate replacement treatment in hypothalamic and pituitary tissue. Both male and female pituitary protein extracts demonstrated an increase in nuclear protein binding activity to a progesterone receptor-oestrogen response element following oestradiol benzoate treatment. However, there was a greater difference in total binding activity seen in the female pituitary extracts compared to male pituitary protein extracts. In both cases, reflecting the binding data, oestradiol benzoate pretreatment led to an increase in pituitary PR-B messenger RNA, although this increase was significantly larger in females than in males. Oestradiol benzoate treatment also led to a significant increase in specific binding of hypothalamic nuclear proteins to the progesterone receptor oestrogen response element from both females and male hypothalamic extracts. In addition, PR-B messenger RNA was induced by oestradiol benzoate treatment in the female rat hypothalamus, under circumstances where no PR-A could be detected. The male also demonstrated an increase in PR-B messenger RNA following oestradiol benzoate treatment, with undetectable levels of PR-A, although to a lesser degree than that seen in the female. The predominance of PR-B over PR-A messenger RNA in rat hypothalamus and pituitary, and the quantitative differences between female and male rats, could both contribute to the greater responsiveness of female rats to progesterone with respect to control over luteinizing hormone release from the pituitary, and lordosis behaviour regulated by hypothalamic neurones. [source]


Oestrogenic Regulation Of Brain Angiotensinogen

JOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2004
K. J. Greenland
Abstract Oestrogens are now recognized as playing a regulatory role on components of the systemic renin,angiotensin system, such as its precursor, angiotensinogen (AGT). In the brain, this role is poorly understood. The aim of this study was to investigate the influence of oestrogens on brain AGT of female rats at different stages of the oestrous cycle, in pregnancy and following ovariectomy with and without hormone replacement. AGT content of different brain regions was also studied in male rats treated with oestrogens. The brain was divided into five regions: cortex, cerebellum, brainstem, midbrain and thalamus/hypothalamus, and AGT was measured by direct radioimmunoassay using a highly specific AGT antibody. Cyclical fluctuations in AGT content were observed in all regions except the cerebellum over the course of the 4-day oestrous cycle, with peak concentrations at estrus and lowest concentrations at metestrus. Following ovariectomy, brain AGT was significantly decreased in the thalamic/hypothalamic region, an effect that was reversed by oestrogen-replacement. In pregnant rats, AGT contents were elevated in the brainstem region. Oestrogen treatment of male rats induced significant increases in AGT concentrations in all areas except the cortex. In summary, these results show that oestradiol has actions on brain AGT that are region-specific and dependent on the particular physiological and reproductive context. Moreover, the changes in AGT concentrations in the oestrous cycle suggest the involvement of other factors besides oestrogen. Finally, this study supports the view that the brain renin,angiotensin system has a broad role in oestrogen-modulated brain functions beyond those specific to the hypothalamic,pituitary,ovarian axis. [source]


Oestrogen Receptor ,-Immunoreactivity in Gonadotropin Releasing Hormone-Expressing Neurones: Regulation by Oestrogen

JOURNAL OF NEUROENDOCRINOLOGY, Issue 9 2001
I. 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]


Oestrogen Promotes Coronary Angiogenesis even under Normoxic Conditions

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2008
Mehdi 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]


Thyrotropin-releasing hormone and oestrogen differentially regulate prolactin and prolactin receptor expression in female human skin and hair follicles in vitro

BRITISH JOURNAL OF DERMATOLOGY, Issue 5 2010
E.A. Langan
Summary Background, Human skin and scalp hair follicles are both a nonclassical target and an extrapituitary source of prolactin (PRL), which is a potent hair growth modulator. However, how the expression of PRL and PRL receptor (PRLR) is regulated in human skin is unknown. Objectives, To investigate whether two key stimulators of pituitary PRL secretion, thyrotropin-releasing hormone (TRH) and oestrogen, also regulate cutaneous PRL and PRLR expression. Methods, Female scalp skin and/or microdissected hair follicles were treated for 6 days in serum-free organ culture with oestrogen (100 nmol L,1), TRH (1,10 ng mL,1, 3,30 nm) or vehicle control. Quantitative immunohistomorphometry of skin and hair follicle sections was complemented with quantitative polymerase chain reaction for PRL and PRLR in cultured hair follicles and/or female human outer root sheath (ORS) keratinocytes. Results, Oestrogen treatment significantly upregulated PRL and PRLR immunoreactivity in selected skin and hair follicle compartments, at the gene and protein level (P < 0·05). TRH significantly increased PRL immunoreactivity and transcription in hair follicles (P < 0·05); however, while it also increased PRLR transcription in hair follicles, it downregulated PRLR immunoreactivity in the hair follicle ORS (P < 0·05). Conclusions, Our pilot study shows that two key endocrine controls of pituitary PRL secretion, oestrogen and TRH, also regulate PRL and PRLR expression in human skin. This provides novel insights into the regulation of extrapituitary PRL and PRLR expression, and invites exploration of oestrogen and TRH as novel therapeutic agents in the management of skin and hair diseases characterized by aberrant PRLR-mediated signalling. [source]


Human mast cells express androgen receptors but treatment with testosterone exerts no influence on IgE-independent mast cell degranulation elicited by neuromuscular blocking agents

EXPERIMENTAL DERMATOLOGY, Issue 3 2010
WenChieh Chen
Please cite this paper as: Human mast cells express androgen receptors but treatment with testosterone exerts no influence on IgE-independent mast cell degranulation elicited by neuromuscular blocking agents. Experimental Dermatology 2010; 19: 302,304. Abstract:, Women predominate in the anaphylactic reactions to neuromuscular blocking agents (NMBA). The expression of oestrogen receptors has been demonstrated in mast cells and oestrogen treatment can enhance mast cell degranulation, but the influence of androgens remains largely unclear. Our immunocytochemical study showed the expression of androgen receptor (AR) in mast cells isolated from human foreskin as well as in two human mast cell lines, HMC-1 and LAD2. The amount of AR was most abundant in human skin mast cells as determined by real-time polymerase chain reaction analysis. Treatment of the HMC-1 mast cells with testosterone or 17,-oestradiol, alone or in combination with different NMBA, did not affect mast cell degranulation as measured by the release of ,-hexosaminidase. Our study shows for the first time the expression of AR in human skin mast cells. Further studies using primary human mast cell cultures are needed to understand whether and how sex hormones can influence mast cell activation. [source]


Health-care problems of Turner syndrome in the adult woman: a cross sectional study of a Victorian cohort and a case for transition

INTERNAL MEDICINE JOURNAL, Issue 1 2006
C. C. Pedreira
Abstract The aim of this study was to assess current care and to survey comorbidity in a cohort of 39 adult women with Turner syndrome in Victoria. Patients with Turner syndrome (TS) drift away from medical care as they achieve adulthood, despite the need for regular surveillance and management of associated conditions, which would reduce morbidity and prevent complications. Clinical assessment was undertaken for 39 women with TS, mean age 30.1 (±11.7) years and information was gathered through personal communication regarding past growth hormone use, oestrogen treatment, hearing loss and health problems. Twenty-four (63.2%) had regular follow-up, but only 17 (43.6%) had adequate recommended surveillance for comorbidities. Forty-three percent had two or more cardiovascular risk factors. Thirty-four (87.2%) were identified with one or more associated disorders. Uterine size was of normal adult dimensions in patients who had received oestrogen before age of 15 years. Adult care for adults with TS is suboptimal and assessment of comorbidities remains sporadic. Adequate transition guidelines and patient education are needed for long-term management of women with TS, to impact on quality of life and longevity. [source]


The Trophic Effects of Oestrogen on Male Rat Anterior Pituitary Lactotrophs

JOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2009
L. 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]


Sex Differences in Oestrogen-Induced p44/42 MAPK Phosphorylation in the Mouse Brain In Vivo

JOURNAL OF NEUROENDOCRINOLOGY, Issue 8 2006
K. Barabás
In addition to the classical direct genomic mechanisms of action, oestrogen also exerts poorly understood, nonclassical effects on the signalling system in neurones. In the present study, we investigated whether sex differences exist in gonadectomy- and oestrogen-induced effects on p44/42 mitogen-activated protein kinase (MAPK) phosphorylation in specific brain regions of mice. We demonstrate that MAPK immunoreactivity was not altered by gonadectomy or oestrogen treatment in either sex. However, we show that the level of phosphorylated MAPK (pMAPK) within the anteroventral periventricular nucleus (AVPV) was consistently higher in males than females irrespective of gonadal steroid hormone status. In addition, gonadectomy was found to decrease pMAPK immunoreactivity within the piriform cortex of males. Oestrogen increased pMAPK immunoreactivity in the medial preoptic area and AVPV of females, but failed to have the same effect in male mice. Overall, these results demonstrate a marked sex difference in oestrogen-induced alteration of MAPK phosphorylation in the brain in vivo. [source]


Cells of the Arcuate Nucleus and Ventromedial Nucleus of the Ovariectomized Ewe that Respond to Oestrogen: A Study Using Fos Immunohistochemistry

JOURNAL OF NEUROENDOCRINOLOGY, Issue 11 2001
I. 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]


Effect of chronic oestrogen administration on androgen receptor expression in reproductive organs and pituitary of adult male rat

ANDROLOGIA, Issue 3 2010
M. C. Kaushik
Summary Following chronic (15 or 30 days) treatment with oestradiol 3-benzoate (75 ,g rat,1 day,1 in 100 ,l of olive oil) to adult rats, androgen receptor (AR) expression was analysed simultaneously in testis, epididymis, seminal vesicle, prostate and pituitary utilising three independent tools i.e. immunohistochemistry, Western blotting and RT-PCR. All the five organs showed higher AR transcriptional activity gradually increasing from 15 to 30 days of oestrogen treatment. However, the AR protein expression either through immunostaining or Western blotting demonstrated a significant decline in all the reproductive organs. In the pituitary, on the other hand, the decline coincided with a distinct breakdown of the AR protein into two bands with increasing duration of treatment. Serum and intra-testicular testosterone levels were found significantly lowered. Spermatogenesis was adversely affected with concurrent decrease in weights of testis and accessory sex organs. Decrease in testis weight was consistent with the reduction in the number of maturing germ cells per tubule. Despite the decrease in weight, accessory sex organs like epididymis, seminal vesicle and prostate were completely devoid of any apoptotic cells which were characterised only in testis and pituitary. Seminiferous epithelium demonstrated a marked increase in the number of germ cells undergoing apoptosis. However, the rate of cell apoptosis was much higher in the pituitary than in the testis at the end of 30 days treatment. It is therefore concluded that degradation of AR protein expression after oestrogen treatment is probably directly linked to an increase in cell apoptosis both in testis and pituitary. [source]


How Oestrogen or Progesterone might Change a woman's susceptibility to HIV-1 infection

AUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 5 2002
Li 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 Conditions

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2008
Mehdi 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 rat

BJU INTERNATIONAL, Issue 6 2004
D.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]