Estrogen receptor transcription and transactivation Basic aspects of estrogen action

Nilsson, Stefan; Gustafsson, Jan Åke

doi:10.1186/bcr81

Cited by 125 publications

(91 citation statements)

References 120 publications

(124 reference statements)

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“…We have shown that serotonin neurons contain exclusively the beta isoform of the ER (ERb), whereas the alpha isoform predominates in the breast and uterus (McLachlan et al, 1992;Nilsson and Gustafsson, 2000;Gundlah et al, 2001b). Hence, it is possible that a ligand with high affinity for ERb could achieve estrogenic actions in the serotonin system without the peripheral risk profile of estradiol.…”

Section: Figurementioning

confidence: 99%

Effects of Ovarian Steroids and Raloxifene on Proteins that Synthesize, Transport, and Degrade Serotonin in the Raphe Region of Macaques

Smith

Henderson

Abell

et al. 2004

Neuropsychopharmacol

150

127

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In the monkey dorsal raphe, we reported that 1-month (mo) of estrogen replacement, with or without progesterone supplementation for 14 days, significantly increased tryptophan hydroxylase-1 (TPH-1) mRNA; decreased serotonin reuptake transporter (SERT) mRNA and decreased monoamine oxidase (MAO)-A mRNA, but had no effect on MAO-B mRNA. Here, we questioned what effect would 1 or 5 mo of ovarian hormones or the selective estrogen receptor modulator (SERM), raloxifene, have on TPH protein and phosphorylation, and on protein expression of SERT, MAO-A or MAO-B? Raloxifene antagonizes estrogen in breast or uterus, but estrogen-like activities in the brain have been reported. Cytoplasmic and membrane extracts of the dorsal raphe region were processed for Western blotting. TPH, phosphoserine, SERT, MAO-A, and MAO-B were detected with specific antibodies. The optical densities of the signals were measured with NIH image and analyzed by ANOVA. Both 1 and 5 mo of estrogen, with or without progesterone, and 5 mo of raloxifene significantly increased TPH protein. Administration for 5 mo of estrogen plus progesterone and raloxifene also increased TPH phosphorylation. Estrogen, with or without progesterone, for 1 mo had no effect on SERT protein. However, 5 mo of estrogen and 5 mo of raloxifene increased SERT protein. Estrogen alone or combined with progesterone for 1 mo caused a significant reduction in MAO-A. Yet, after 5 mo of the same treatments, MAO-A was not different from spayed controls. Estrogen alone had no effect on MAO-B. However, the addition of progesterone significantly increased MAO-B. Raloxifene for 5 mo had no effect on MAO-A or MAO-B. Thus, to various extents, estrogen, progesterone, and raloxifene may increase serotonin production and transport. The expression of the degradative enzymes suggests a complex combination of gene transcription, post-transcriptional processing, and substrate feedback mechanisms.

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Section: Figurementioning

confidence: 99%

Effects of Ovarian Steroids and Raloxifene on Proteins that Synthesize, Transport, and Degrade Serotonin in the Raphe Region of Macaques

Smith

Henderson

Abell

et al. 2004

Neuropsychopharmacol

150

127

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“…7 More recently, studies have also demonstrated an antioxidant effect by estrogen, reducing LDL oxidation in vivo and in vitro. 43 The direct effects of estrogen on the vascular system and which modulate the vascular tonus comprise 1) acute vasodilatation, increasing the synthesis and bioactivity of nitric oxide; 44,45 2) long-term modulation of vascular tonus, regulating the production of prostaglandins and expression of eNOS and the endothelin gene 46 ; 3) inhibition of endothelin-induced vasoconstriction 47 ; and 4) inhibition of sympathetic activity. 27 In addition to these actions on the vascular tonus, estrogen exerts an antiproliferative action on the vascular smooth layer.…”

Section: Estrogen Menopause and Endothelial Functionmentioning

confidence: 99%

Menopause, Estrogens, and Endothelial Dysfunction: Current Concepts

Maturana

Irigoyen

Spritzer

2007

Clinics

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Maturana MA, Irigoyen MC, Spritzer PM. Menopause, estrogens, and endothelial dysfunction: current concepts. Clinics. 2007;62(1):77-86. Menopause is defined as the permanent cessation of menses. Cardiovascular disease is the leading cause of death among postmenopausal women in developed countries. The disparity between the incidence of cardiovascular disease among women in pre-and postmenopause has been ascribed to the actions of endogenous estrogen on the cardiovascular system and, particularly, on the vascular endothelium. The endothelium plays an important role in cardiovascular homeostasis, either through the vascular tonus and its regulation, or through coagulation and the inflammatory response. Endothelial dysfunction is implicated in the genesis of atherosclerosis and other chronic disorders, such as diabetes mellitus and hypertension. The pharmacological use of estrogen exerts influence on the circulating levels of markers of vascular tonus, and inflammation, as well as prothrombotic, and fibrinolytic markers, but the impact of these changes on the atherosclerotic disease is still uncertain.

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“…These 2 receptors are the products of 2 distinct genes (22) that are believed to have unique functions in the body (23). They may be simultaneously present in some organs and tissues, whereas in other organs one of the ER types dominates over the other (24)(25)(26).…”

Section: Introductionmentioning

confidence: 99%

Estrogen receptor β protects against acoustic trauma in mice

Meltser

Tahera

Simpson³

et al. 2008

J. Clin. Invest.

141

117

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The hormone estradiol affects the auditory system both by itself and by its interaction with neuroprotective factors. In this study, we examined the role of estrogen receptors (ERs) in response to auditory trauma. We found a ligand-dependent protective role for ERβ in the auditory system by investigating mice deficient in ERα (ERKO mice), ERβ (BERKO mice), and aromatase (ARKO mice). Basal auditory brainstem response (ABR) thresholds were similar in all animals. An acoustic trauma causing a temporary hearing loss raised ABR thresholds in male and female BERKO and ARKO mice compared with WT and ERKO mice. The ERα-selective agonist, propyl(1H) pyrazole-1,3,5-triyl-trisphenol (PPT), partially protected ARKO mice from trauma, while the ERβ-selective agonist, 2,3-bis (4-hydroxyphenyl)-propionitrile (DPN), protected WT and ARKO mice. Immunohistochemistry and western blotting confirmed the expression of ERβ in cochlea of WT males and females. Levels of brain-derived neurotrophic factor (BDNF), a neuroprotective peptide that can be induced by estrogen, was lower in BERKO and ARKO mice compared with WT. DPN treatment increased BDNF expression in ARKO mice. These data indicate ERβ-mediated neuroprotection involving BDNF in the auditory system of males and females.

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Estrogen receptor transcription and transactivation Basic aspects of estrogen action

Cited by 125 publications

References 120 publications

Effects of Ovarian Steroids and Raloxifene on Proteins that Synthesize, Transport, and Degrade Serotonin in the Raphe Region of Macaques

Effects of Ovarian Steroids and Raloxifene on Proteins that Synthesize, Transport, and Degrade Serotonin in the Raphe Region of Macaques

Menopause, Estrogens, and Endothelial Dysfunction: Current Concepts

Estrogen receptor β protects against acoustic trauma in mice

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