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Estrogen Signaling (estrogen + signaling)
Terms modified by Estrogen Signaling Selected AbstractsAlcohol-Induced Disruption of Endocrine SignalingALCOHOLISM, Issue 8 2007Martin J. J. Ronis This article contains the proceedings of a symposium at the 2006 ISBRA Meeting in Sydney Australia, organized and cochaired by Martin J. Ronis and Thomas M. Badger. The presentations were (1) Effect of Long-Term Ethanol Consumption on Liver Injury and Repair, by Jack R. Wands; (2) Alcohol-Induced Insulin Resistance in Liver: Potential Roles in Regulation of ADH Expression, Ethanol Clearance, and Alcoholic Liver Disease, by Thomas M. Badger; (3) Chronic Gestational Exposure to Ethanol Causes Brain Insulin and Insulin-Like Growth Factor Resistance, by Suzanne M de la Monte; (4) Disruption of IGF-1 Signaling in Muscle: A Mechanism Underlying Alcoholic Myopathy, by Charles H. Lang; (5) The Role of Reduced Plasma Estradiol and Impaired Estrogen Signaling in Alcohol-Induced Bone Loss, by Martin J. Ronis; and (6) Short-Term Influence of Alcohol on Appetite-Regulating Hormones in Man, by Jan Calissendorff. [source] Estrogen signaling and disruption of androgen metabolism in acquired androgen-independence during cadmium carcinogenesis in human prostate epithelial cellsTHE PROSTATE, Issue 2 2007Lamia Benbrahim-Tallaa Abstract BACKGROUND Lethal prostate cancers often become androgen-independent due to androgen receptor (AR) overexpression. The role of cadmium in prostate tumor progression was determined. METHODS Control and cadmium-transformed prostate epithelial cells (CTPE) were compared for steroid-induced proliferation, steroid receptor expression, and androgen metabolism. RESULTS CTPE cells showed rapid proliferation in complete medium and sustained proliferation in steroid-reduced medium. Androgens stimulated significantly less cell proliferation and AR-related genes expression in CTPE cells. 5,-Dihydrotestosterone increased PSA expression more effectively in control cells. Flutamide reduced 5,-dihydrotestosterone-stimulated growth less effectively in CTPE cells compared to control. CTPE cells showed decreased p27 expression. Estrogen receptors were overexpressed and estradiol markedly stimulated proliferation in CTPE cells. In CTPE cells 5,-aromatase was markedly increased, while 5,-reductase was decreased. CONCLUSIONS Cadmium-induced malignant transformation stimulates androgen independence, unrelated to AR expression or activity. Increased estrogen receptor and 5,-aromatase expression suggest estrogen signaling may be critical to this process. Prostate © 2006 Wiley-Liss, Inc. [source] CYP7B1-mediated metabolism of dehydroepiandrosterone and 5,-androstane-3,,17,-diol , potential role(s) for estrogen signalingFEBS JOURNAL, Issue 8 2008Hanna Pettersson CYP7B1, a cytochrome P450 enzyme, metabolizes several steroids involved in hormonal signaling including 5,-androstane-3,,17,-diol (3,-Adiol), an estrogen receptor agonist, and dehydroepiandrosterone, a precursor for sex hormones. Previous studies have suggested that CYP7B1-dependent metabolism involving dehydroepiandrosterone or 3,-Adiol may play an important role for estrogen receptor ,-mediated signaling. However, conflicting data are reported regarding the influence of different CYP7B1-related steroids on estrogen receptor , activation. In the present study, we investigated CYP7B1-mediated conversions of dehydroepiandrosterone and 3,-Adiol in porcine microsomes and human kidney cells. As part of these studies, we compared the effects of 3,-Adiol (a CYP7B1 substrate) and 7,-hydroxy-dehydroepiandrosterone (a CYP7B1 product) on estrogen receptor , activation. The data obtained indicated that 3,-Adiol is a more efficient activator, thus lending support to the notion that CYP7B1 catalysis may decrease estrogen receptor , activation. Our data on metabolism indicate that the efficiencies of CYP7B1-mediated hydroxylations of dehydroepiandrosterone and 3,-Adiol are very similar. The enzyme catalyzed both reactions at a similar rate and the Kcat/Km values were in the same order of magnitude. A high dehydroepiandrosterone/3,-Adiol ratio in the incubation mixtures, similar to the ratio of these steroids in many human tissues, strongly suppressed CYP7B1-mediated 3,-Adiol metabolism. As the efficiencies of CYP7B1-mediated hydroxylation of dehydroepiandrosterone and 3,-Adiol are similar, we propose that varying steroid concentrations may be the most important factor determining the rate of CYP7B1-mediated metabolism of dehydroepiandrosterone or 3,-Adiol. Consequently, tissue-specific steroid concentrations may have a strong impact on CYP7B1-dependent catalysis and thus on the levels of different CYP7B1-related steroids that can influence estrogen receptor , signaling. [source] Evidence for non-genomic transmission of ecological information via maternal behavior in female ratsGENES, BRAIN AND BEHAVIOR, Issue 1 2007J. McLeod Maternal behavior is flexible and programs offspring development. Using a novel manipulation, we demonstrate that rat maternal behavior is sensitive to ecologically relevant stimuli. Long-Evans hooded rat dams (F0) and pups were exposed to a predator condition (cat odor) or a control condition (no odor) for 1 h on the day of parturition. Predator-exposed F0 dams displayed significantly more maternal behavior (licking/grooming, arched-back nursing) relative to control-exposed dams across five subsequent observation days. Female offspring (F1) were raised to adulthood, bred and maternal behavior was observed. F1 dams reared by a predator-exposed F0 dam displayed significantly higher maternal behavior relative to F1 dams reared by a control-exposed F0 dam across 5 days of observation. Increased levels of maternal behavior in predator-reared (PR) F1 dams were evident even in F1 females that had been cross-fostered (CF) from a control-exposed F0 dam, suggesting a non-genomic transmission of increased levels of maternal behavior. Lactating PR F1 dams had significantly elevated estrogen receptor , and , mRNA in the medial preoptic area relative to control-reared (CR) F1 dams. Furthermore, among CR F1 dams, there was no significant difference between those dams that had been CF from predator-exposed F0 dams and those that had been sham CF. These results support the hypothesis that flexible rat maternal behavior can shape offspring development according to current environmental conditions. The results also suggest that estrogen signaling may be part of an epigenetic mechanism by which changes in maternal behavior are passed from F0 to F1 dams. [source] Dietary sources of lignans and isoflavones modulate responses to estradiol in estrogen reporter miceMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 8 2009Pauliina E. Penttinen-Damdimopoulou Abstract Dietary phytoestrogens, such as the lignan metabolite enterolactone (ENL) and the isoflavone genistein (GEN), are suggested to modulate the risk of estrogen-dependent disease (e.g., breast cancer) through regulation of estrogen signaling. However, the effects of complex food items containing lignans or isoflavones on estrogen receptor (ER) transactivation have not been assessed so far. In this study, the modulation of ER-mediated signaling by dietary sources of lignans (cereals and flaxseed) and isoflavones (soy) was studied in vivo. Adult ovariectomized 3×ERE-luciferase (luc) reporter mice received isocaloric diets supplemented with flaxseed, rye, wheat, or soy for 40 h or two weeks, and an additional group of mice was challenged with 17,-estradiol (E2) following the two-week dietary intervention. In non-E2 -treated mice, soy diet induced luc expression in liver, mammary gland, and pituitary gland while the other diets had no effects. Interestingly, all diets modulated the E2 -induced luc expression. In particular rye diet efficiently reduced E2 -induced luc expression as well as uterine growth, the hallmark of estrogen action in vivo. It is concluded that dietary sources of lignans and isoflavones can modulate estrogen signaling in vivo. The results suggest intriguing possibilities for the modulation of the risk of estrogen-dependent diseases by dietary means. [source] Role of dietary lignans in the reduction of breast cancer riskMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 7 2007Niina M. Saarinen Abstract Lignans are a large group of fiber-associated phenolic compounds widely distributed in edible plants. Some of the ingested plant lignans are converted by intestinal microbiota to enterolignans, enterodiol (END) and enterolactone (ENL), the latter of which has been thought to be the major biologically active lignan, and suggested to be associated with low risk of breast cancer. In line with this, administration of plant lignans which are further metabolized to ENL, or ENL as such, have been shown to inhibit or delay the growth of experimental mammary cancer. The mechanism of anticarcinogenic action of ENL is not yet fully understood, but there is intriguing evidence for ENL as a modulator of estrogen signaling. These findings have generated interest in the use of lignans as components of breast cancer risk reducing functional foods. Identification of target groups, who would benefit most, is of pivotal importance. Therefore, further identification and validation of relevant biomarkers, which can be used as indicators of lignan or ENL action and breast cancer risk reduction at different stages of the disease, are of importance. [source] Thyroid hormone and reproduction: Regulation of estrogen receptors in goldfish gonadsMOLECULAR REPRODUCTION & DEVELOPMENT, Issue 9 2010Erik R. Nelson Abstract There is increasing evidence that thyroid hormones influence reproduction in vertebrates. However, little information is available on the mechanisms by which this happens. As a first step in determining these mechanisms, we test the hypothesis that the estrogen receptor subtypes (ER,, ER,-1, and ER,-2) are regulated by the thyroid hormone, (T3), in the gonads of goldfish. All three subtypes were down-regulated by T3 in the testis or ovary. We also found evidence that T3 decreased pituitary gonadotropin expression and decreased transcript for gonadal aromatase. Collectively, it appears that T3 acts to diminish estrogen signaling by (1) decreasing pituitary LH expression and thus steroidogenesis, (2) down-regulating gonadal aromatase expression and thus decreasing estrogen synthesis from androgens, and (3) decreasing sensitivity to estrogen by down-regulating the ER subtypes. Goldfish are seasonal breeders, spawning once a year, and thus have two distinct periods of growth: somatic and reproductive. Circulating thyroid hormone levels have been found to increase just after spawning. Therefore, we propose that this may be an endocrine mechanism that goldfish use to switch their energy expenditure from reproductive to growth efforts in the goldfish. Mol. Reprod. Dev. 77: 784,794, 2010. © 2010 Wiley-Liss, Inc. [source] Estrogen signaling and disruption of androgen metabolism in acquired androgen-independence during cadmium carcinogenesis in human prostate epithelial cellsTHE PROSTATE, Issue 2 2007Lamia Benbrahim-Tallaa Abstract BACKGROUND Lethal prostate cancers often become androgen-independent due to androgen receptor (AR) overexpression. The role of cadmium in prostate tumor progression was determined. METHODS Control and cadmium-transformed prostate epithelial cells (CTPE) were compared for steroid-induced proliferation, steroid receptor expression, and androgen metabolism. RESULTS CTPE cells showed rapid proliferation in complete medium and sustained proliferation in steroid-reduced medium. Androgens stimulated significantly less cell proliferation and AR-related genes expression in CTPE cells. 5,-Dihydrotestosterone increased PSA expression more effectively in control cells. Flutamide reduced 5,-dihydrotestosterone-stimulated growth less effectively in CTPE cells compared to control. CTPE cells showed decreased p27 expression. Estrogen receptors were overexpressed and estradiol markedly stimulated proliferation in CTPE cells. In CTPE cells 5,-aromatase was markedly increased, while 5,-reductase was decreased. CONCLUSIONS Cadmium-induced malignant transformation stimulates androgen independence, unrelated to AR expression or activity. Increased estrogen receptor and 5,-aromatase expression suggest estrogen signaling may be critical to this process. Prostate © 2006 Wiley-Liss, Inc. [source] | |||||||||||||