Ginecol Obstet Mex. 2003 Nov;71:585-9.
[High concentrations of serum estradiol in assisted reproduction]
[Article in Spanish]
Saucedo de la Llata E, Moraga Sanchez MR, Pezino Rodriguez J, Trevino A, Leal Almeida M, Sepulveda J, Arenas Montezco L, Garcia Villafana G, Batiza Resendiz VA, Santos Haliscak R, Galache Vega P, Hernandez Ayup S.
Instituto para el Estudio de la Concepcion Humana, Monterrey, NL.
OBJECTIVES: To analyze the influence of the levels of estradiol on the day of HCG in the pregnancy rate (PR) of ICSI and oocyte donation. STUDY DESIGN: Retrospective, comparative. MATERIAL AND METHODS: 333 patients underwent ICSI and 66 in oocyte donation were included dividing them according to the level of estradiol: a) < 1,000 pg/mL, b) 1,001-3,000 pg/mL and c) > 3,000 pg/mL. Therapeutic protocol: Down regulation with acetate leuprolide in late luteal phase, COH with FSHr and/or HMG, ultrasonographic monitoring and estradiol blood levels, HCG application with > 3 follicles > 18 mm, oocyte retrieval 34 hours later. We analyzed: PR, age (including receptors), FSH and LH. Number, mature grade and fertilized oocytes; luteal support, transfer quality and type of catheter. Statistical analysis (SPSS 11) with chi square, ANOVA and Kruskall-Wallis. RESULTS: ICSI: Older patients in group A (p < 0.001), but without difference between B and C groups (p = 0.08). Statistical difference in number of follicles, number of oocytes, fertilized oocytes and transferred embryos being less in the A group (p < 0.001). Statistical difference in PR 21.7, 35.6 and 25.7% in A, B and C groups respectively (p = 0.032). Oocyte donation: Group A has younger patients (p = 0.005), FSH and LH were similiar among groups. Major number of follicles were observed to increase estradiol levels, but major quantity of metaphase II and fertilized oocytes were observed in group B (p = 0.05). PR without significant differences: 50, 51.5 and 52.3% in groups A, B and C (p = 0.977). Without statistical differen
Arterioscler Thromb Vasc Biol. 2004 Sep;24(9):1628-33. Epub 2004 Jul 01.
Estrogen, heat shock proteins, and NFkappaB in human vascular endothelium.
Hamilton KL, Mbai FN, Gupta S, Knowlton AA.
Baylor College of Medicine, Houston, Tex., USA.
BACKGROUND: We hypothesized that estrogen would increase HSP72 in human coronary artery endothelial cells (HCAEC), and that these would be more sensitive to estrogen than our previous observations in myocytes. METHODS AND RESULTS: HCAEC were treated with 17beta-estradiol or tamoxifen, ranging from physiological to pharmacological(1 nM to 10 micromol/L) for either 24 hours (early) or 7 days (chronic). HSP expression was assessed by Western blots. Both early and chronic 17beta-estradiol and tamoxifen increased HSP72. Electromobility shift assays (EMSA) showed activation of HSF-1 with early, but not chronic, 17beta-estradiol. 17beta-Estradiol activated NFkappaB within 10 minutes, and the ER-alpha selective inhibitor, ICI 182 780, abolished this effect. Transcription factor decoys containing the heat shock element blocked HSP72 induction. Estrogen pretreatment decreased lactate dehydrogenase release with hypoxia. This protective effect persisted despite blockade of HSF-1 by decoys. However, an NF-kappaB decoy prevented the increase in HSP72 and abolished the estrogen-associated protection during hypoxia. CONCLUSIONS: 17beta-Estradiol upregulates HSP72 early and chronically via different mechanisms in HCAEC, and provides cytoprotection during hypoxia, independent of HSP72 induction. NF-kappaB mediates the early increase in HSP72, suggesting that estrogen activates NF-kappaB via a nongenomic, receptor-dependent mechanism, and this leads to activation of HSF-1. Activation of NF-kappaB was critical for estrogen-associated protection. Further studies are needed to elucidate the involved signaling pathways. We hypothesized that estrogen would increase HSP72 in human coronary artery endothelial cells (HCAEC). Both early and chronic treatment increased HSP72. EMSA showed activation of HSF-1 with ear
Osteoporos Int. 2004 Nov;15(11):909-917. Epub 2004 Jul 3.
Role of sex steroids in the regulation of bone morphology in men. The MINOS study.
Szulc P, Uusi-Rasi K, Claustrat B, Marchand F, Beck TJ, Delmas PD.
INSERM Research Unit 403, Hopital Edouard Herriot, Place d'Arsonval, 69437, Lyon, France.
In ageing men, skeletal fragility is associated with reduced cortical thickness and decreased bone density. To better understand the role of testosterone and 17beta-estradiol regarding these characteristics of skeletal fragility, we correlated their circulating levels with the estimates of mechanical bone properties derived from areal bone mineral density (aBMD) measured by DXA. External diameter and BMD were used to estimate cortical thickness, cross-sectional area (CSA), section modulus, buckling ratio and strength index of the femoral neck and distal radius on 760 men aged 40-85 years. The 17beta-estradiol level was an independent positive determinant of CSA, aBMD and estimated cortical thickness of both bones. In multivariate models adjusted for age, body weight, height, lean body mass and testosterone concentration, men in the lowest quartile of 17beta-estradiol had lower CSA at the femoral neck (4.8%, P<0.001) and distal radius (3.6%, P<0.01) compared with men in the highest quartile. They had also thinner cortical bone at the femoral neck and distal radius (4.8%, P<0.001 and 4.6%, P<0.001, respectively). Furthermore 17beta-estradiol had a negative association with indices of cortical instability (buckling ratio) and a positive association with bending strength (section modulus, strength index) both at femoral neck and radius. Men in the lowest quartile of 17beta-estradiol had higher buckling ratios (femoral neck 4.8%, P<0.002; radius 5.1%, P<0.005), lower strength index (femoral neck 8.5%, P<0.001, radius 6.1%, P<0.01) and greater section modulus at the femoral neck. However, there were no between-quartile differences in external diameter in any bone sites. Similar, even though somewha
J Clin Endocrinol Metab. 2004 Jul;89(7):3261-9.
Endogenous sex hormones, sex hormone-binding globulin, and the risk of incident vertebral fractures in elderly men and women: the Rotterdam Study.
Goderie-Plomp HW, van der Klift M, de Ronde W, Hofman A, de Jong FH, Pols HA.
Department of Internal Medicine, Erasmus Medical Center, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands. h.polrasmusmc.nl
In an age-matched, case-control study, we investigated the association between endogenous sex steroid hormones and incident vertebral fractures in both elderly men and women (aged 67.7 +/- 6.8 yr). Drawn from the Rotterdam Study, participants required radiographs of the lumbar spine at both baseline and follow-up (average time of follow-up, 6.5 yr) and frozen blood samples, taken at baseline. One hundred and seventy-eight men (45 cases) and 454 women (115 cases) were thus selected. Serum estradiol, SHBG, testosterone, and insulin were measured, along with bone mineral density at both spine and hip. Women in the lowest tertile of serum estradiol (< or =15.5 pmol/liter) had a 2.1 times increased risk (95% confidence interval, 1.3-3.5) of incident vertebral fractures, independently of bone mineral density measured at either site. SHBG levels in the lowest two tertiles were associated with a 50% reduction in incident vertebral fracture risk. Women with a combination of both low estradiol and high SHBG had a 7.8 times higher risk of an incident vertebral fracture (95% confidence interval, 2.7-22.5; P < 0.001), adjusted for age and weight. This increased risk did not change when non-SHBG-bound estradiol was used instead of total estradiol. For men, no clear association was found, possibly due to insufficient power. No clear association between testosterone and incident vertebral fractures was observed in either men or women.
J Cardiovasc Pharmacol. 2004 Aug;44(2):155-63.
Daidzein and 17 beta-estradiol enhance nitric oxide synthase activity associated with an increase in calmodulin and a decrease in caveolin-1.
Woodman OL, Missen MA, Boujaoude M.
Department of Pharmacology, University of Melbourne, Victoria, Australia. owenlnimelb.edu.au
Isoflavones, such as daidzein, are proposed to possess vasculoprotective properties, perhaps through a mechanism similar to estrogen. Our experiments aimed to test the hypothesis that daidzein and 17 beta-estradiol enhance endothelium-dependent relaxation through an increase in NO synthesis due to an increase in activity or expression of endothelial nitric oxide synthase (eNOS). Male rats were treated with daidzein (0.2 mg/kg per day sc), 17 beta-estradiol (0.1 mg/kg per day sc), or vehicle for 7 days and reactivity of isolated aortic rings was then determined. ACh-induced relaxation was significantly enhanced in aortic rings from rats treated with daidzein or 17 beta-estradiol but the relaxant responses to the endothelium-independent dilators sodium nitroprusside or isoprenaline were not different. Nitrite production and the level of cGMP were significantly greater in aortae from daidzein and 17 beta-estradiol compared with vehicle-treated rats. Daidzein and 17 beta-estradiol did not alter eNOS protein in endothelium-intact aortae but reduced expression of caveolin-1 and increased expression of calmodulin, changes that would account for an increase in eNOS activity. There were no differences between groups in the expression of calmodulin and caveolin-1 in arteries when the endothelium was removed. Daidzein or 17 beta-estradiol treatment selectively enhances endothelium-dependent relaxation in male rats through an increase in eNOS activity. The increase in eNOS activity is associated with a decreased expression of caveolin-1 and an increased expression of calmodulin in endothelial cells.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15243295&dopt=Abstract estradiol [PubMed - in process]
Eur J Neurosci. 2004 Jul;20(1):217-28.
Oestrogen-deficient female aromatase knockout (ArKO) mice exhibit depressive-like symptomatology.
Dalla C, Antoniou K, Papadopoulou-Daifoti Z, Balthazart J, Bakker J.
Centre for Cellular and Molecular Neurobiology, University of Liege, Liege, Belgium.
We recently found that female aromatase knockout (ArKO) mice that are deficient in oestradiol due to a targeted mutation in the aromatase gene show deficits in sexual behaviour that cannot be corrected by adult treatment with oestrogens. We determined here whether these impairments are associated with changes in general levels of activity, anxiety or 'depressive-like' symptomatology due to chronic oestrogen deficiency. We also compared the neurochemical profile of ArKO and wild-type (WT) females, as oestrogens have been shown to modulate dopaminergic, serotonergic and noradrenergic brain activities. ArKO females did not differ from WT in spontaneous motor activity, exploration or anxiety. These findings are in line with the absence of major neurochemical alterations in hypothalamus, prefrontal cortex or striatum, which are involved in the expression of these behaviours. By contrast, ArKO females displayed decreased active behaviours, such as struggling and swimming, and increased passive behaviours, such as floating, in repeated sessions of the forced swim test, indicating that these females exhibit 'depressive-like' symptoms. Adult treatment with oestradiol did not reverse the behavioural deficits observed in the forced swim test, suggesting that they may be due to the absence of oestradiol during development. Accordingly, an increased serotonergic activity was observed in the hippocampus of ArKO females compared with WT, which was also not reversed by adult oestradiol treatment. The possible organizational role of oestradiol on the hippocampal serotonergic system and the 'depressive-like' profile of ArKO females provide new insights into the pathophysiology of depression and the increased vulnerability
Indian J Exp Biol. 2003 Jul;41(7):748-55.
Expression and regulation of integrin receptors in human trophoblast cells: role of estradiol and cytokines.
Das C, Basak S.
Department of Biochemistry, All India Institute of Medical Sciences, Ansari Nagar, New Delhi 110 029, India. chandana_otmail.com
Embryo implantation and placentation are dynamic cellular events that require not only synchrony between the maternal environment and the embryo, but also complex cell-cell communication amongst the implanting blastocyst and the receptive endometrium through integrins, a large family of proteins involved in the attachment, migration, invasion and control of cellular functions. Integrins display dynamic temporal and spatial patterns of expression by the trophoblast cells during early pregnancy in humans. However, the precise mechanism of embryo implantation and the modulation of the integrin receptors during blastocyst attachment and further implantation remain elusive in the humans. The present study elucidates the expression and hormonal modulation of fibronectin, vitronectin and laminin integrin receptors by estradiol and IL-1alpha in human trophoblast cells. Human first trimester trophoblast cells showed the induction of the classical estrogen receptor (ER)-alpha by its own ligand, estradiol. Treatment with either estradiol or IL-1alpha induced the expressions of alpha4, alpha5, alpha6 and alpha(v) integrin receptor subunits at both the mRNA and protein levels, while expression of beta1 remained unaltered. Furthermore, estradiol upregulated the expression of IL-1alpha, thereby suggesting the possibility that estrogen may either directly or via the proinflammatory cytokine induces the expression of the cell surface integrin receptors. The findings delineate the role of hormones and the cytokines in modulating the adhesiveness and attachment of the trophoblast cells. This may reflect the in vivo scenario where the implanting embryo is surrounded by a hormone-cytokine rich uterine microenvironment t
Horm Behav. 2004 Aug;46(2):158-64.
Different effects of subchronic doses of 17-beta estradiol in two ethologically based models of anxiety utilizing female rats.
Koss WA, Gehlert DR, Shekhar A.
Program in Medical Neurobiology, Department of Psychiatry, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Estrogen may have differing effects on 'anxiety' responses under different conditions. The current study tested the effects of estrogen on anxiety-like behavior when administered for 6-7 days in ovariectomized (OVX) female rats. Two animal paradigms were utilized; the elevated plus maze (EPM), measuring changes in innate fear of exploration of open spaces; and the social interaction test (SIT), measuring the exploration of a novel, same gender partner. In the EPM, estradiol-treated OVX females both entered and spent more time in the open arms than control OVX females, indicating an anxiolytic-like action of estradiol. In contrast, estradiol treated OVX females interacted less with the partner animal in the SIT compared with controls suggesting anxiogenic-like effects. The possible anxiogenic effect of estradiol in the SIT is supported by two findings: (1) the effect is reversed by the anxiolytic drug alprazolam and (2) estrogen did not affect locomotion and therefore, the reduced social interaction is not due to reduced activity. Acute administration of progesterone (5 mg/kg), which has anxiolytic properties, did not reverse estradiol-induced social interaction deficits, suggesting that lack of progesterone did not account for estradiol's anxiogenic effects. These results, while seemingly contradictory when interpreted within a unified concept of anxiety, may well reflect the ethological roles of reproductive hormones and their effects on different types of exploratory anxiety.
Pflugers Arch. 2004 Jul 16 [Epub ahead of print]
Oestradiol rapidly inhibits Ca(2+) signals in ciliary neurons through classical oestrogen receptors in cytoplasm.
Viso-Leon MC, Ripoll C, Nadal A.
Institut de Bioenginyeria, Universitat Miguel Hernandez d'Elx, Campus de Sant Joan, Carretera Alacant-Valencia Km 87, 03550, Sant Joan d'Alacant, Spain.
Oestrogen plays a key role in a great variety of actions in the nervous system, either through classical or alternative pathways. The classical pathways are initiated after oestrogen binding to the oestrogen receptors ERalpha or ERbeta, which translocate from the cytoplasm to the nucleus and act there as transcription factors. Alternative pathways are initiated at the plasma membrane and cytoplasm, via binding to classical or non-classical ERs. Using isolated ciliary ganglion neurons from the chick embryo and Ca(2+) imaging, we demonstrated that a 10-min exposure to 17beta-oestradiol reduces Ca(2+) influx through the plasma membrane. This effect was not reproduced by oestradiol conjugated to bovine serum albumin, which does not cross the plasma membrane, indicating that 17beta-oestradiol was acting intracellularly. ERalpha was detected in the cytoplasm by immunostaining and its involvement in the regulation of Ca(2+) influx by ICI182,780 inhibition. The phosphatidylinositol-3 kinase (PI3-kinase) inhibitor wortmannin and the nitric oxide synthase (NOS) inhibitor N(omega)-nitro- l-arginine methyl ester (L-NAME) both blocked the oestradiol effect. The oestradiol effect was reproduced by 8Br-cGMP and abolished in the presence of the cGMP-dependent protein kinase (PKG) inhibitor KT5823. Our study indicates that 17beta-oestradiol can regulate Ca(2+) influx via PI3-kinase, NOS and PKG after activation of cytoplasmic ER.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15258764&dopt=Abstract estradiol [PubMed - as supplied by publisher]
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