Journal articles on the topic 'Hormones, Sex – Receptors'
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1
Honma, Naoko, Yoko Matsuda, and Tetuo Mikami. "Carcinogenesis of Triple-Negative Breast Cancer and Sex Steroid Hormones." Cancers 13, no. 11 (May 25, 2021): 2588. http://dx.doi.org/10.3390/cancers13112588.
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Triple-negative breast cancer (TNBC) lacks an effective treatment target and is usually associated with a poor clinical outcome; however, hormone unresponsiveness, which is the most important biological characteristic of TNBC, only means the lack of nuclear estrogenic signaling through the classical estrogen receptor (ER), ER-α. Several sex steroid receptors other than ER-α: androgen receptor (AR), second ER, ER-β, and non-nuclear receptors represented by G-protein-coupled estrogen receptor (GPER), are frequently expressed in TNBC and their biological and clinical importance has been suggested by a large number of studies. Despite the structural similarity between each sex steroid hormone (androgens and estrogens) or each receptor (AR and ER-β), and similarity in the signaling mechanisms of these hormones, most studies or reviews focused on one of these receptors, and rarely reviewed them in a comprehensive way. Considering the coexistence of these hormones and their receptors in TNBC in a clinical setting, a comprehensive viewpoint would be important to correctly understand the association between the carcinogenic mechanism or pathobiology of TNBC and sex steroid hormones. In this review, the carcinogenic or pathobiological role of sex steroid hormones in TNBC is considered, focusing on the common and divergent features of the action of these hormones.
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Zarazúa, Abraham, Aliesha González-Arenas, Gabriela Ramírez-Vélez, Blanca Bazán-Perkins, Christian Guerra-Araiza, and María G. Campos-Lara. "Sexual Dimorphism in the Regulation of Estrogen, Progesterone, and Androgen Receptors by Sex Steroids in the Rat Airway Smooth Muscle Cells." International Journal of Endocrinology 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/8423192.
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The role of sex hormones in lung is known. The three main sex steroid receptors, estrogen, progesterone, and androgen, have not been sufficiently studied in airway smooth muscle cells (ASMC), and the sex hormone regulation on these receptors is unknown. We examined the presence and regulation of sex hormone receptors in female and male rat ASMC by Western blotting and flow cytometry. Gonadectomized rats were treated with 17β-estradiol, progesterone, 17β-estradiol + progesterone, or testosterone. ASMC were enzymatically isolated from tracheas and bronchi. The experiments were performed with double staining flow cytometry (anti-α-actin smooth muscle and antibodies to each hormone receptor). ERα, ERβ, tPR, and AR were detected in females or males. ERαwas upregulated by E2 and T and downregulated by P4 in females; in males, ERαwas downregulated by P4, E + P, and T. ERβwas downregulated by each treatment in females, and only by E + P and T in males. tPR was downregulated by P4, E + P, and T in females. No hormonal regulation was observed in male receptors. AR was downregulated in males treated with E + P and T. We have shown the occurrence of sex hormone receptors in ASMC and their regulation by the sex hormones in female and male rats.
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Baber, Rod. "Sex hormones, receptors and modulators." Australian and New Zealand Journal of Obstetrics and Gynaecology 57, no. 4 (August 2017): 391–92. http://dx.doi.org/10.1111/ajo.12666.
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Orshal, Julia M., and Raouf A. Khalil. "Gender, sex hormones, and vascular tone." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 286, no. 2 (February 2004): R233—R249. http://dx.doi.org/10.1152/ajpregu.00338.2003.
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The greater incidence of hypertension and coronary artery disease in men and postmenopausal women compared with premenopausal women has been related, in part, to gender differences in vascular tone and possible vascular protective effects of the female sex hormones estrogen and progesterone. However, vascular effects of the male sex hormone testosterone have also been suggested. Estrogen, progesterone, and testosterone receptors have been identified in blood vessels of human and other mammals and have been localized in the plasmalemma, cytosol, and nuclear compartments of various vascular cells, including the endothelium and the smooth muscle. The interaction of sex hormones with cytosolic/nuclear receptors triggers long-term genomic effects that could stimulate endothelial cell growth while inhibiting smooth muscle proliferation. Activation of plasmalemmal sex hormone receptors may trigger acute nongenomic responses that could stimulate endothelium-dependent mechanisms of vascular relaxation such as the nitric oxide-cGMP, prostacyclin-cAMP, and hyperpolarization pathways. Additional endothelium-independent effects of sex hormones may involve inhibition of the signaling mechanisms of vascular smooth muscle contraction such as intracellular Ca2+ concentration and protein kinase C. The sex hormone-induced stimulation of the endothelium-dependent mechanisms of vascular relaxation and inhibition of the mechanisms of vascular smooth muscle contraction may contribute to the gender differences in vascular tone and may represent potential beneficial vascular effects of hormone replacement therapy during natural and surgically induced deficiencies of gonadal hormones.
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Fannon, Stacey A., Regina M. Vidaver, and Sherry A. Marts. "Historical Perspectives: An abridged history of sex steroid hormone receptor action." Journal of Applied Physiology 91, no. 4 (October 1, 2001): 1854–59. http://dx.doi.org/10.1152/jappl.2001.91.4.1854.
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The field of steroid hormone action is well established, although it is barely more than four decades old. Pivotal experiments in the late 1950s and 1960s showed that hormone-binding components exist within nuclei of target tissues and that steroid hormones act by regulating gene expression, rather than directly influencing enzymatic processes. The understanding that steroid hormone receptors interact with the general transcription machinery and alter chromatin structure came in the 1970s and 1980s, and details of this mechanism continue to be elucidated. In addition, the discovery of rapid cellular responses to steroid hormones has led to the identification of putative membrane-bound steroid receptors that act without affecting gene transcription. As noted in the recent Institute of Medicine report Exploring the Biological Contributions to Human Health: Does Sex Matter?, the effects of steroid hormones and defects in steroid hormone receptor action have a profound impact on human health and disease. Future research directives include the development of potent, selective steroid receptor modulators, the elucidation of nongenomic steroid hormone effects, and further exploration of hormone-genome interactions.
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Simão, Vinícius Augusto, Luiz Gustavo de Almeida Chuffa, and Isabel Cristina Cherici Camargo. "Ovarian sex steroid receptors and sex hormones in androgenized rats." Reproduction 152, no. 5 (November 2016): 545–59. http://dx.doi.org/10.1530/rep-16-0233.
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This study evaluated for the first time the effects of different doses of the anabolic steroid nandrolone decanoate (ND) on the expression of ovarian steroid receptors (AR, ER-α (ESR1) and ER-β (ESR2)) and related sex hormones after treatment and recovery periods in adult rats. The animals were injected subcutaneously with doses of ND (1.87, 3.75, 7.5 or 15 mg/kg b.w.) or mineral oil (control group) for 15 days, and the experimental groups were divided into three periods of evaluation: (a) ND treatment for 15 days, (b) ND treatment and recovery for a period of 30 days and (c) ND treatment and recovery for a period of 60 days. Estrous cycle was monitored daily. At the end of each period, rats were killed for collection of blood and ovaries. Persistent diestrus occurred in all rats during ND treatment and after 30-day recovery. The highest dose of ND was able to maintain all rats arrested at diestrus until 60-day recovery. The expression of steroid receptors varied in a dose- and period-dependent manner, having a more pronounced response with the dose of 15 mg ND/kg. ND treatment increased serum levels of testosterone, 17β-estradiol and dihydrotestosterone, especially at the highest doses of 7.5 and 15 mg ND/kg. No change was observed in the levels of follicle-stimulating hormone (FSH), whereas levels of the luteinizing hormone (LH) varied according to the dose and period. In conclusion, the ovarian sex steroid receptors and sex hormones were restored only at lower doses of ND and after a longer period of recovery.
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Bhatia, Aruna, Harmandeep Kaur Sekhon, and Gurpreet Kaur. "Sex Hormones and Immune Dimorphism." Scientific World Journal 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/159150.
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The functioning of the immune system of the body is regulated by many factors. The abnormal regulation of the immune system may result in some pathological conditions. Sex hormones of reproductive system are one of the major factors that regulate immune system due to the presence of hormone receptors on immune cells. The interaction of sex hormones and immune cells through the receptors on these cells effect the release of cytokines which determines the proliferation, differentiation, and maturation of different types of immunocytes and as a result the outcome of inflammatory or autoimmune diseases. The different regulations of sex hormones in both sexes result in immune dimorphism. In this review article the mechanism of regulation of immune system in different sexes and its impact are discussed.
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Simoncini, T., and AR Genazzani. "Non-genomic actions of sex steroid hormones." European Journal of Endocrinology 148, no. 3 (March 1, 2003): 281–92. http://dx.doi.org/10.1530/eje.0.1480281.
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Steroid hormone receptors have been traditionally considered to act via the regulation of transcriptional processes, involving nuclear translocation and binding to specific response elements, and ultimately leading to regulation of gene expression. However, novel non-transcriptional mechanisms of signal transduction through steroid hormone receptors have been identified. These so-called 'non-genomic' effects do not depend on gene transcription or protein synthesis and involve steroid-induced modulation of cytoplasmic or cell membrane-bound regulatory proteins. Several relevant biological actions of steroids have been associated with this kind of signaling. Ubiquitous regulatory cascades such as mitogen-activated protein kinases, the phosphatidylinositol 3-OH kinase and tyrosine kinases are modulated through non-transcriptional mechanisms by steroid hormones. Furthermore, steroid hormone receptor modulation of cell membrane-associated molecules such as ion channels and G-protein-coupled receptors has been shown. TIssues traditionally considered as 'non-targets' for classical steroid actions are instead found to be vividly regulated by non-genomic mechanisms. To this aim, the cardiovascular and the central nervous system provide excellent examples, where steroid hormones induce rapid vasodilatation and neuronal survival via non-genomic mechanisms, leading to relevant pathophysiological consequences. The evidence collected in the past Years indicates that target cells and organs are regulated by a complex interplay of genomic and non-genomic signaling mechanisms of steroid hormones, and the integrated action of these machineries has important functional roles in a variety of pathophysiological processes. The understanding of the molecular basis of the rapid effects of steroids is therefore important, and may in the future turn out to be of relevance for clinical purposes.
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Higa, Gerald M., and Ryan G. Fell. "Sex Hormone Receptor Repertoire in Breast Cancer." International Journal of Breast Cancer 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/284036.
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Classification of breast cancer as endocrine sensitive, hormone dependent, or estrogen receptor (ER) positive refers singularly to ERα. One of the oldest recognized tumor targets, disruption of ERα-mediated signaling, is believed to be the mechanistic mode of action for all hormonal interventions used in treating this disease. Whereas ERαis widely accepted as the single most important predictive factor (for response to endocrine therapy), the presence of the receptor in tumor cells is also of prognostic value. Even though the clinical relevance of the two other sex hormone receptors, namely, ERβand the androgen receptor remains unclear, two discordant phenomena observed in hormone-dependent breast cancers could be causally related to ERβ-mediated effects and androgenic actions. Nonetheless, our understanding of regulatory molecules and resistance mechanisms remains incomplete, further compromising our ability to develop novel therapeutic strategies that could improve disease outcomes. This review focuses on the receptor-mediated actions of the sex hormones in breast cancer.
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Villablanca, Amparo C., Muthuvel Jayachandran, and Carole Banka. "Atherosclerosis and sex hormones: current concepts." Clinical Science 119, no. 12 (September 1, 2010): 493–513. http://dx.doi.org/10.1042/cs20100248.
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CVD (cardiovascular disease) is the leading cause of death for women. Considerable progress has been made in both our understanding of the complexities governing menopausal hormone therapy and our understanding of the cellular and molecular mechanisms underlying hormone and hormone receptor function. Understanding the interplay of atherosclerosis and sex steroid hormones and their cognate receptors at the level of the vessel wall has important ramifications for clinical practice. In the present review, we discuss the epidemiology of CVD in men and women, the clinical impact of sex hormones on CVD, and summarize our current understanding of the pathogenesis of atherosclerosis with a focus on gender differences in CVD, its clinical presentation and course, and pathobiology. The critical animal and human data that pertain to the role of oestrogens, androgens and progestins on the vessel wall is also reviewed, with particular attention to the actions of sex hormones on each of the three key cell types involved in atherogenesis: the endothelium, smooth muscle cells and macrophages. Where relevant, the systemic (metabolic) effects of sex hormones that influence atherogenesis, such as those involving vascular reactivity, inflammation and lipoprotein metabolism, are discussed. In addition, four key current concepts in the field are explored: (i) total hormone exposure time and coronary heart disease risk; (ii) the importance of tissue specificity of sex steroid hormones, critical timing and the stage of atherosclerosis in hormone action; (iii) biomarkers for atherosclerosis with regard to hormone therapy; and (iv) the complex role of sex steroids in inflammation. Future studies in this field will contribute to guiding clinical treatment recommendations for women and help define research priorities.
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Hillerns, Pablo Ibieta, Yuangang Zu, and Michael Wink. "Binding of Phytoestrogens to Rat Uterine Estrogen Receptors and Human Sex Hormone-binding Globulins." Zeitschrift für Naturforschung C 60, no. 7-8 (August 1, 2005): 649–56. http://dx.doi.org/10.1515/znc-2005-7-823.
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The interaction of phytoestrogens with the most important binding sites of steroid hormones, i.e. sex hormone-binding globulin and estrogen receptors, was investigated. Relative binding affinities and association constants for 21 compounds among them isoflavones, flavones, flavonols, flavanones, chalcones and lignans were determined. The lignan nordihydroguaiaretic acid weakly displaced 17β-[3H]-estradiol from estrogen receptor and Scatchard analysis suggests non-conformational changes. Compounds from Glycyrrhiza glabra, liquiritigenin and isoliquiritigenin, showed estrogenic affinities to both receptors. 18β-Glycyrrhetinic acid displaced 17β-[3H]-estradiol from sex hormone-binding globulin but not from the estrogen receptor. Phytoestrogens compete with 17β-estradiol much stronger than with 5α-dihydrotestosterone for binding to sex hormone-binding globulin.
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Shen, Minqian, and Haifei Shi. "Sex Hormones and Their Receptors Regulate Liver Energy Homeostasis." International Journal of Endocrinology 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/294278.
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The liver is one of the most essential organs involved in the regulation of energy homeostasis. Hepatic steatosis, a major manifestation of metabolic syndrome, is associated with imbalance between lipid formation and breakdown, glucose production and catabolism, and cholesterol synthesis and secretion. Epidemiological studies show sex difference in the prevalence in fatty liver disease and suggest that sex hormones may play vital roles in regulating hepatic steatosis. In this review, we summarize current literature and discuss the role of estrogens and androgens and the mechanisms through which estrogen receptors and androgen receptors regulate lipid and glucose metabolism in the liver. In females, estradiol regulates liver metabolism via estrogen receptors by decreasing lipogenesis, gluconeogenesis, and fatty acid uptake, while enhancing lipolysis, cholesterol secretion, and glucose catabolism. In males, testosterone works via androgen receptors to increase insulin receptor expression and glycogen synthesis, decrease glucose uptake and lipogenesis, and promote cholesterol storage in the liver. These recent integrated concepts suggest that sex hormone receptors could be potential promising targets for the prevention of hepatic steatosis.
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Ziller, Nadja, Roland Kotolloshi, Mohsen Esmaeili, Marita Liebisch, Ralf Mrowka, Aria Baniahmad, Thomas Liehr, Gunter Wolf, and Ivonne Loeffler. "Sex Differences in Diabetes- and TGF-β1-Induced Renal Damage." Cells 9, no. 10 (October 3, 2020): 2236. http://dx.doi.org/10.3390/cells9102236.
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While females are less affected by non-diabetic kidney diseases compared to males, available data on sex differences in diabetic nephropathy (DN) are controversial. Although there is evidence for an imbalance of sex hormones in diabetes and hormone-dependent mechanisms in transforming growth factor β1 (TGF-β1) signaling, causes and consequences are still incompletely understood. Here we investigated the influence of sex hormones and sex-specific gene signatures in diabetes- and TGF-β1-induced renal damage using various complementary approaches (a db/db diabetes mouse model, ex vivo experiments on murine renal tissue, and experiments with a proximal tubular cell line TKPTS). Our results show that: (i) diabetes affects sex hormone concentrations and renal expression of their receptors in a sex-specific manner; (ii) sex, sex hormones and diabetic conditions influence differences in expression of TGF-β1, its receptor and bone morphogenetic protein 7 (BMP7); (iii) the sex and sex hormones, in combination with variable TGF-β1 doses, determine the net outcome in TGF-β1-induced expression of connective tissue growth factor (CTGF), a profibrotic cytokine. Altogether, these results suggest complex crosstalk between sex hormones, sex-dependent expression pattern and profibrotic signals for the precise course of DN development. Our data may help to better understand previous contradictory findings regarding sex differences in DN.
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Freedman, Robert R., and Rachael Baer. "Sex Hormones Modulate Peripheral Vascular Adrenergic Receptors." Menopause 3, no. 4 (1996): 225. http://dx.doi.org/10.1097/00042192-199603040-00035.
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Venken, K., F. Callewaert, S. Boonen, and D. Vanderschueren. "Sex hormones, their receptors and bone health." Osteoporosis International 19, no. 11 (April 5, 2008): 1517–25. http://dx.doi.org/10.1007/s00198-008-0609-z.
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HILPERT, Jan, Henrik VORUM, Regina BURMEISTER, Robert SPOELGEN, Irina GRISHKOVSKAYA, Rolf MISSELWITZ, Anders NYKJAER, and Thomas E. WILLNOW. "Efficient eukaryotic expression system for authentic human sex hormone-binding globulin." Biochemical Journal 360, no. 3 (December 10, 2001): 609–15. http://dx.doi.org/10.1042/bj3600609.
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Sex hormone-binding globulin (SHBG) is the main carrier for androgens and oestrogens in humans. It mediates the transport of steroid hormones in the circulation and testicular fluid, and regulates their bioavailability to steroid-responsive tissues. In addition, the protein interacts with membrane receptors expressed in target tissues. Binding to the receptors is suspected to facilitate the uptake of steroid hormones and/or elicit cellular signal transduction. The identity of the SHBG receptor has not yet been resolved, in part due to a lack of sufficient quantities of authentic SHBG for receptor purification and molecular characterization. We have successfully addressed this problem by establishing an episomal expression system in human embryonic kidney cells that produces 5mg of fully active human SHBG per litre. The recombinant protein resembles native SHBG in terms of structure, glycosylation pattern and steroid-binding activity. Moreover, the protein interacts with plasma membranes in steroid target tissues, an activity not observed with SHBG from other recombinant expression systems. Thus our studies have removed an important obstacle to the further elucidation of the role SHBG plays in steroid hormone action.
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Shramko, S. V., L. F. Gulyaeva, V. N. Zorina, and T. V. Tretyakova. "Proliferative diseases of the uterus: clinical, immunological, and molecular aspects." Voprosy ginekologii, akušerstva i perinatologii 19, no. 5 (2020): 13–21. http://dx.doi.org/10.20953/1726-1678-2020-5-13-21.
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Objective. To perform comparative analysis of clinical data, serum levels of acute-phase proteins, cytokines, steroid hormones, and expression of genes encoding sex hormone receptors in tissues of patients with proliferative diseases of the uterus. Patients and methods. We analyzed clinical data of 349 patients with various proliferative diseases of the uterus. We also evaluated their serum levels of α2-macroglobulin, pregnancy-associated α2-glycoprotein, their immunocomplexes with IgG, lactoferrin, VEGF, IL-6, TNFa, IL-8, and sex hormones. Uterine tissue samples were tested for the expression of genes encoding estrogen receptors α and β (ЕRα, ЕRβ) and progesterone receptors (PGR). Data analysis was performed using the statistical packages of SAS 9.4, STATISTICA12, and IBM-SPSS Statistics 22. Results. The changes in the level of acute-phase proteins indicated inflammation. In isolated uterine fibroids, expression of genes encoding progesterone receptors prevailed, whereas in isolated adenomyosis, expression of genes encoding estrogen receptors prevailed. Patients with both uterine fibroids and adenomyosis demonstrated similar levels of expression of genes encoding sex steroid hormone receptors. Tissues of uterine leiomyosarcoma were characterized by downregulated expression of genes encoding sex steroid hormone receptors. Conclusion. Upregulation of genes encoding progesterone receptors in isolated uterine fibroids confirms that therapy with progesterone receptor blockers is appropriate in this case. The predominance of expression of genes encoding estrogen receptors in isolated adenomyosis indicates local hyperestrogenism, justifying the use of progestogens and antiestrogens. Equal expression of genes encoding estrogen and progesterone receptors in patients with combined disease, as wells as high frequency of inflammatory changes in tissues and increased serum levels of inflammatory markers, proves the need for antiinflammatory therapy. Key words: adenomyosis, inflammation, steroid receptor genes, leiomyosarcoma, uterine fibroids, gene expression
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Mariotti, Angelo. "Sex Steroid Hormones and Cell Dynamics in the Periodontium." Critical Reviews in Oral Biology & Medicine 5, no. 1 (January 1994): 27–53. http://dx.doi.org/10.1177/10454411940050010201.
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The biological changes that occur in tissues of the periodontium during puberty, the menstrual cycle, pregnancy, menopause, and oral contraceptive use have heightened interest in the relationship between sex steroid hormones and periodontal health. These clinical observations coupled with tissue specificity of hormone localization, identification of hormone receptors, as well as the metabolism of hormones have strongly suggested that periodontal tissues are targets for androgens, estrogens, and progestins. The etiologies of periodontal endocrinopathies are diverse; nonetheless, periodontal pathologies may be a consequence of the actions and interactions of sex steroid hormones on specific cells found in the periodontium.
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Regitz-Zagrosek, Vera, and Georgios Kararigas. "Mechanistic Pathways of Sex Differences in Cardiovascular Disease." Physiological Reviews 97, no. 1 (January 2017): 1–37. http://dx.doi.org/10.1152/physrev.00021.2015.
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Major differences between men and women exist in epidemiology, manifestation, pathophysiology, treatment, and outcome of cardiovascular diseases (CVD), such as coronary artery disease, pressure overload, hypertension, cardiomyopathy, and heart failure. Corresponding sex differences have been studied in a number of animal models, and mechanistic investigations have been undertaken to analyze the observed sex differences. We summarize the biological mechanisms of sex differences in CVD focusing on three main areas, i.e., genetic mechanisms, epigenetic mechanisms, as well as sex hormones and their receptors. We discuss relevant subtypes of sex hormone receptors, as well as genomic and nongenomic, activational and organizational effects of sex hormones. We describe the interaction of sex hormones with intracellular signaling relevant for cardiovascular cells and the cardiovascular system. Sex, sex hormones, and their receptors may affect a number of cellular processes by their synergistic action on multiple targets. We discuss in detail sex differences in organelle function and in biological processes. We conclude that there is a need for a more detailed understanding of sex differences and their underlying mechanisms, which holds the potential to design new drugs that target sex-specific cardiovascular mechanisms and affect phenotypes. The comparison of both sexes may lead to the identification of protective or maladaptive mechanisms in one sex that could serve as a novel therapeutic target in one sex or in both.
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Sherwood, Nancy M., Bruce A. Adams, and Javier A. Tello. "Endocrinology of protochordates." Canadian Journal of Zoology 83, no. 1 (January 1, 2005): 225–55. http://dx.doi.org/10.1139/z04-178.
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Large-scale gene duplications occurred early in the vertebrate lineage after the split with protochordates. Thus, protochordate hormones and their receptors, transcription factors, and signaling pathways may be the foundation for the endocrine system in vertebrates. A number of hormones have been identified including cionin, a likely ancestor of cholecytokinin (CCK) and gastrin. Both insulin and insulin-like growth hormone (IGF) have been identified in separate cDNAs in a tunicate, whereas only a single insulin-like peptide was found in amphioxus. In tunicates, nine distinct forms of gonadotropin-releasing hormone (GnRH) are shown to induce gamete release, even though a pituitary gland and sex steroids are lacking. In both tunicates and amphioxus, there is evidence of some components of a thyroid system, but the lack of a sequenced genome for amphioxus has slowed progress in the structural identification of its hormones. Immunocytochemistry has been used to tentatively identify a number of hormones in protochordates, but structural and functional studies are needed. For receptors, protochordates have many vertebrate homologs of nuclear receptors, such as the thyroid, retinoic acid, and retinoid X receptors. Also, tunicates have cell surface receptors including the G-protein-coupled type, such as β-adrenergic, putative endocannabinoid, cionin (CCK-like), and two GnRH receptors. Several tyrosine kinase receptors include two epidermal growth factor (EGF) receptors (tunicates) and an insulin/IGF receptor (amphioxus). Interestingly, neither steroid receptors nor a full complement of enzymes for synthesis of sex steroids are encoded in the Ciona genome. Tunicates appear to have some but not all of the necessary molecules to develop a vertebrate-like pituitary or complete thyroid system.
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Vegeto, Elisabetta, Alessandro Villa, Sara Della Torre, Valeria Crippa, Paola Rusmini, Riccardo Cristofani, Mariarita Galbiati, Adriana Maggi, and Angelo Poletti. "The Role of Sex and Sex Hormones in Neurodegenerative Diseases." Endocrine Reviews 41, no. 2 (September 23, 2019): 273–319. http://dx.doi.org/10.1210/endrev/bnz005.
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Abstract Neurodegenerative diseases (NDs) are a wide class of disorders of the central nervous system (CNS) with unknown etiology. Several factors were hypothesized to be involved in the pathogenesis of these diseases, including genetic and environmental factors. Many of these diseases show a sex prevalence and sex steroids were shown to have a role in the progression of specific forms of neurodegeneration. Estrogens were reported to be neuroprotective through their action on cognate nuclear and membrane receptors, while adverse effects of male hormones have been described on neuronal cells, although some data also suggest neuroprotective activities. The response of the CNS to sex steroids is a complex and integrated process that depends on (i) the type and amount of the cognate steroid receptor and (ii) the target cell type—either neurons, glia, or microglia. Moreover, the levels of sex steroids in the CNS fluctuate due to gonadal activities and to local metabolism and synthesis. Importantly, biochemical processes involved in the pathogenesis of NDs are increasingly being recognized as different between the two sexes and as influenced by sex steroids. The aim of this review is to present current state-of-the-art understanding on the potential role of sex steroids and their receptors on the onset and progression of major neurodegenerative disorders, namely, Alzheimer’s disease, Parkinson’s diseases, amyotrophic lateral sclerosis, and the peculiar motoneuron disease spinal and bulbar muscular atrophy, in which hormonal therapy is potentially useful as disease modifier.
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Yamashina, Masahiro, Takahiro Tsutsui, Yoshihisa Sei, Munetaka Akita, and Michito Yoshizawa. "A polyaromatic receptor with high androgen affinity." Science Advances 5, no. 4 (April 2019): eaav3179. http://dx.doi.org/10.1126/sciadv.aav3179.
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Biological receptors distinguish and bind steroid sex hormones, e.g., androgen-, progestogen-, and estrogen-type hormones, with high selectivity. To date, artificial molecular receptors have been unable to discriminate between these classes of biosubstrates. Here, we report that an artificial polyaromatic receptor preferentially binds a single molecule of androgenic hormones, known as “male” hormones (indicated with m), over progestogens and estrogens, known as “female” hormones (indicated with f), in water. Competitive experiments established the binding selectivity of the synthetic receptor for various sex hormones to be testosterone (m) > androsterone (m) >> progesterone (f) > β-estradiol (f) > pregnenolone (f) > estriol (f). These bindings are driven by the hydrophobic effect, and the observed selectivity arises from multiple CH-π contacts and hydrogen-bonding interactions in the semirigid polyaromatic cavity. Furthermore, micromolar fluorescence detection of androgen was demonstrated using the receptor containing a fluorescent dye in water.
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Meikle, A., C. Tasende, C. Sosa, and E. G. Garófalo. "The role of sex steroid receptors in sheep female reproductive physiology." Reproduction, Fertility and Development 16, no. 4 (2004): 385. http://dx.doi.org/10.1071/rd04036.
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Cell responsiveness to steroid hormones is related to the number and affinity of its receptors, thus factors affecting steroid expression will influence tissue sensitivity and functionality. The present review discusses the role of oestrogen and progesterone receptors in sheep female reproductive physiology. The mechanism of steroid hormone action in the target cell is introduced first; the tissue distribution, physiological functions and regulation of oestrogen receptor subtypes and progesterone receptor isoforms in ruminants are reported. The role of steroid receptors in target tissues (with emphasis on the uterus and pituitary gland) during different physiological events is addressed in an attempt to clarify oestrogen and progesterone actions in different developmental and reproductive stages: prepubertal period, oestrous cycle, pregnancy, post-partum period and seasonal anoestrus. The present review shows how the distinct reproductive stages are accompanied by dramatic changes in uterine receptor expression. The role of oestrogen and progesterone receptors in the molecular mechanism responsible for premature luteolysis that results in subnormal luteal function is discussed. Finally, the effect of nutrition on sex steroid receptor expression and the involvement on reproductive performance is reported.
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Mukudai, Shigeyuki, Ken Ichi Matsuda, Takeshi Nishio, Yoichiro Sugiyama, Hideki Bando, Ryuichi Hirota, Hirofumi Sakaguchi, Yasuo Hisa, and Mitsuhiro Kawata. "Differential Responses to Steroid Hormones in Fibroblasts From the Vocal Fold, Trachea, and Esophagus." Endocrinology 156, no. 3 (March 1, 2015): 1000–1009. http://dx.doi.org/10.1210/en.2014-1605.
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Abstract There is accumulating evidence that fibroblasts are target cells for steroids such as sex hormones and corticoids. The characteristics of fibroblasts vary among tissues and organs. Our aim in this study is to examine differences in responses to steroid hormones among fibroblasts from different cervicothoracic regions. We compared the actions of steroid hormones on cultured fibroblasts from the vocal folds, which are considered to be the primary target of steroid hormones, and the trachea and esophagus in adult male rats. Expression of steroid hormone receptors (androgen receptor, estrogen receptor α, and glucocorticoid receptor) was identified by immunofluorescence histochemistry. Androgen receptor was much more frequently expressed in fibroblasts from the vocal fold than in those from the trachea and esophagus. Cell proliferation analysis showed that administration of testosterone, estradiol, or corticosterone suppressed growth of all 3 types of fibroblasts. However, mRNA expression for extracellular matrix–associated genes, including procollagen I and III and elastin, and hyaluronic acid synthase I was elevated only by addition of testosterone to fibroblasts from the vocal fold. These results indicate that each steroid hormone exerts region-specific effects on cervicothoracic fibroblasts with different properties through binding to specific receptors.
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Ayakannu, Thangesweran, Anthony H. Taylor, Timothy H. Marczylo, Jonathon M. Willets, and Justin C. Konje. "The Endocannabinoid System and Sex Steroid Hormone-Dependent Cancers." International Journal of Endocrinology 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/259676.
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The “endocannabinoid system (ECS)” comprises the endocannabinoids, the enzymes that regulate their synthesis and degradation, the prototypical cannabinoid receptors (CB1 and CB2), some noncannabinoid receptors, and an, as yet, uncharacterised transport system. Recent evidence suggests that both cannabinoid receptors are present in sex steroid hormone-dependent cancer tissues and potentially play an important role in those malignancies. Sex steroid hormones regulate the endocannabinoid system and the endocannabinoids prevent tumour development through putative protective mechanisms that prevent cell growth and migration, suggesting an important role for endocannabinoids in the regulation of sex hormone-dependent tumours and metastasis. Here, the role of the endocannabinoid system in sex steroid hormone-dependent cancers is described and the potential for novel therapies assessed.
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Norstedt, G., B. Husman, A. Mode, P. Eneroth, U. J. Lewis, and J. Å. Gustafsson. "Induction of prolactin receptors in the liver is more closely related to the growth-promoting than to the lactogenic potency of peptides." Acta Endocrinologica 114, no. 3 (March 1987): 350–56. http://dx.doi.org/10.1530/acta.0.1140350.
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Abstract. The sex differentiated binding 125I-human prolactin (PRL) to rat liver membranes was studied and the present results extend our previous studies on induction of hepatic PRL receptors by growth hormone (GH). In prepubertal female rats, PRL receptor levels are low compared with those in mature female rat livers. Infusion of hGH during one week to 17-day-old female rats resulted in a receptor level typical of adult female rats. The time course of receptor disappearance in male rats treated with hGH was also studied. When the receptor-inducing hormone was removed, receptor levels in hGH-treated male rats returned to the normal level characteristic of male rats after approximately 96 h. The specificity of various GH-like and PRL-like hormones in PRL receptor induction was studied in hypophysectomized rats. The PRL-like hormones were identified by measuring their potency to displace 125I-hPRL from a receptor preparation obtained from female rat livers, and the GH-like hormones were identified by their potency to increase body weight in hypophysectomized rats. Using similar doses of hormones it was found that in vivo administration of growth-promoting peptides (rGH, hGH, bGH) induced PRL receptors, whereas lactogenic hormones (rPRL, hPL) had a very small or no effect on PRL receptor induction. This suggests that binding to a type of GH receptor is the first step in PRL receptor induction.
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Ismail, Ahmed, Katarzyna Anna Mierzejewska, Anna Janowska-Wieczorek, A. Robert Turner, Mariusz Z. Ratajczak, and Magdalena Kucia. "Novel Evidence That Pituitary Gonadotropins Directly Stimulate Human Leukemic cells—studies on Myeloid Cell Lines and Primary Patient AML and CML Cells." Blood 124, no. 21 (December 6, 2014): 2204. http://dx.doi.org/10.1182/blood.v124.21.2204.2204.
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Abstract Background . It has been postulated that hematopoietic stem/progenitor cells (HSPCs) can become specified from a population of migrating primordial germ cells (PGCs) isolated from embryos. In support of this intriguing possibility, HSPCs and PGCs are both highly migratory populations of stem cells, and evidence has accumulated for the sharing of several mutated genes (e.g., Sall4) as well as chromosomal aberrations between germline tumors and leukemias or lymphomas, which suggests their common clonal origin. In fact, we recently observed that normal murine HSPCs express several functional receptors for pituitary gonadal hormones, such as follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin (PRL), in addition to gonadal hormones including estrogens, androgen, and progesterone. Of note, the plasma levels of FSH and LH are elevated in older patients, which correlate with an increase in the incidence of myeloid leukemia. Hypothesis . Based on this, we have hypothesized that gonadotropic hormones play a yet underappreciated role in human malignant hematopoiesis. Materials and Methods . To address this issue, we performed a complex series of experiments employing human myeloid hematopoietic cell lines (KG-1a, K-562, U937, THP-1, HEL) and primary patient cells (AML, CML) to address the influence of pituitary sex hormones (FSH, LH, PRL) as well as gonadal sex hormones (androgen, estrogen, progesterone) on proliferation, migration, and adhesion of malignant cells. In addition, expression of the corresponding receptors was evaluated at the mRNA level by PCR, and their functionality was confirmed by signaling studies based on phosphorylation of major signal transduction pathways (AKT, MAPKp42/44, STAT). Results. We demonstrate for the first time that human myeloid leukemia cell lines express all pituitary gonadotropin and several gonadal hormone receptors and that FSH and LH receptors are functional on these cells, as evaluated by chemotaxis and adhesion assays. Moreover, FSH and LH receptors were expressed and functional on patient leukemic blasts in bone marrow (BM) and peripheral blood (PB). Human leukemic cells from cell lines and primary patient-derived cells also expressed some other gonadal hormone receptors (PRL-R, estrogen, progesterone, and androgen receptors), albeit at lower levels. Moreover, we observed that several human myeloid cell lines as well as primary patient leukemic cells responded to sex hormones by proliferation. Conclusions . Our data are the first to indicate that pituitary-secreted gonadotropins stimulate migration, adhesion, and proliferation of leukemic cells. This latter effect seems to be direct, as the receptors for these hormones respond to stimulation by phosphorylation of intracellular pathways involved in cell proliferation. Established human myeloid leukemia cell lines and primary patient blasts also responded to stimulation by gonadal sex hormones. Finally, our studies provide further evidence supporting a developmental link between hematopoiesis and the germline. Disclosures No relevant conflicts of interest to declare.
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Wierman, Margaret E. "Sex steroid effects at target tissues: mechanisms of action." Advances in Physiology Education 31, no. 1 (January 2007): 26–33. http://dx.doi.org/10.1152/advan.00086.2006.
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Our understanding of the mechanisms of sex hormone action has changed dramatically over the last 10 years. Estrogens, progestins, and androgens are the steroid hormones that modulate reproductive function. Recent data have shown that many other tissues are targets of sex hormones in addition to classical reproductive organs. This review outlines new advances in our understanding of the spectrum of steroid hormone ligands, newly recognized target tissues, structure-function relationships of steroid receptors, and, finally, their genomic and nongenomic actions. Sex-based specific effects are often related to the different steroid hormone mileu in men compared with women. Understanding the mechanisms of sex steroid action gives insight into the differences in normal physiology and disease states.
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Kur, Paulina, Agnieszka Kolasa-Wołosiuk, Kamila Misiakiewicz-Has, and Barbara Wiszniewska. "Sex Hormone-Dependent Physiology and Diseases of Liver." International Journal of Environmental Research and Public Health 17, no. 8 (April 11, 2020): 2620. http://dx.doi.org/10.3390/ijerph17082620.
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Sexual dimorphism is associated not only with somatic and behavioral differences between men and women, but also with physiological differences reflected in organ metabolism. Genes regulated by sex hormones differ in expression in various tissues, which is especially important in the case of liver metabolism, with the liver being a target organ for sex hormones as its cells express estrogen receptors (ERs: ERα, also known as ESR1 or NR3A; ERβ; GPER (G protein-coupled ER, also known as GPR 30)) and the androgen receptor (AR) in both men and women. Differences in sex hormone levels and sex hormone-specific gene expression are mentioned as some of the main variations in causes of the incidence of hepatic diseases; for example, hepatocellular carcinoma (HCC) is more common in men, while women have an increased risk of autoimmune liver disease and show more acute liver failure symptoms in alcoholic liver disease. In non-alcoholic fatty liver disease (NAFLD), the distinction is less pronounced, but increased incidences are suggested among men and postmenopausal women, probably due to an increased tendency towards visceral fat accumulation.
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García-Gómez, Elizabeth, Bertha González-Pedrajo, and Ignacio Camacho-Arroyo. "Role of Sex Steroid Hormones in Bacterial-Host Interactions." BioMed Research International 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/928290.
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Sex steroid hormones play important physiological roles in reproductive and nonreproductive tissues, including immune cells. These hormones exert their functions by binding to either specific intracellular receptors that act as ligand-dependent transcription factors or membrane receptors that stimulate several signal transduction pathways. The elevated susceptibility of males to bacterial infections can be related to the usually lower immune responses presented in males as compared to females. This dimorphic sex difference is mainly due to the differential modulation of the immune system by sex steroid hormones through the control of proinflammatory and anti-inflammatory cytokines expression, as well as Toll-like receptors (TLRs) expression and antibody production. Besides, sex hormones can also affect the metabolism, growth, or virulence of pathogenic bacteria. In turn, pathogenic, microbiota, and environmental bacteria are able to metabolize and degrade steroid hormones and their related compounds. All these data suggest that sex steroid hormones play a key role in the modulation of bacterial-host interactions.
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Vermeirsch, Hilde, Wim Van Den Broeck, Mark Coryn, and Paul Simoens. "Immunolocalization of sex steroid hormone receptors in the canine uterine tube and their relation to sex steroid hormone levels." Reproduction, Fertility and Development 14, no. 4 (2002): 241. http://dx.doi.org/10.1071/rd01084.
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The aim of this immunohistochemical study was to describe the cellular distribution of the estrogen receptor-α (ERα), progesterone receptor (PR) and androgen receptor (AR) in canine uterine tubes. Samples of uterine tubes were taken from dogs in different stages of the estrous cycle, and dogs that were pregnant or had just delivered. Nuclear staining for sex steroid hormone receptors was observed in the surface epithelium, stromal cells and smooth muscle cells of the muscular layer. Only slight differences in staining pattern were observed between the ampulla and fimbriae. The staining for ERα and PR showed changes throughout the estrous cycle. Some of these changes were related to changing concentrations of sex steroid hormones. High staining scores for ERα and PR were found during proestrus and low scores during early metestrus. The staining for AR showed only minor cyclic changes. However, during proestrus and estrus, cytoplasmic staining for AR was observed in differentiated secretory epithelial cells, when nuclear staining in these cells was nearly absent. For the three hormone receptors, stromal cells generally stained with a higher intensity than epithelial cells. It is likely that many steroid hormone actions on the epithelium are mediated through stromal cells. During pregnancy, rather high staining scores were found for ERα and AR in the uterine tube. This is in contrast to observations in the canine pregnant uterus.
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Nagasue, Naofumi, and Hitoshi Kohno. "Hepatocellular Carcinoma and Sex Hormones." HPB Surgery 6, no. 1 (January 1, 1992): 1–6. http://dx.doi.org/10.1155/1992/72761.
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The liver is morphologically and functionally modulated by sex hormones. Long-term use of oral contraceptives and androgenic steroids can induce benign and malignant hepatocellular tumors. Hepatocellular carcinoma (HCC) is more prevalent in men than in women. The role of sex hormones and their receptors in the development of HCC was reviewed. Some HCCs may be androgen dependent but others may be estrogen or even both dependent. Further studies are mandatory in order to utilize such characteristics of HCC for an effective prophylaxis and therapy of this tumor.
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Dzieciuchowicz, L., M. Kotwicka, M. Gabriel, A. Szczęśniak-Chmielecka, B. Krasińska, G. Oszkinis, W. Majewski, and Z. Krasiński. "Sex hormone receptors in varicose veins of women with premenstrual syndrome." Phlebologie 37, no. 02 (March 2008): 68–72. http://dx.doi.org/10.1055/s-0037-1622215.
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SummaryThe pathogenesis of premenstrual tension syndrome is not fully understood. It has been hypothesized that the interaction between sex hormones and target organs is the key event in its pathogenesis. Aim: The purpose of the study was to examine the differences in the prevalence of smooth muscle cells with sex hormones receptors in varicose veins of women with and without premenstrual tension syndrome (PS). Patients, methods: Samples of great saphenous vein were obtained from 50 women during varicose vein surgery. They were divided into group I (20 women with clinically diagnosed PS) and group II (30 women without PS). Estrogen and progesterone receptors were detected with an immunohistochemical method. Superficial densities of smooth muscle cells positive to estrogen and progesterone receptors were analyzed with densitometric program IM-AN and automatic image analyzer Magicall. The results were compared with t-Student test. Results: There were no differences in superficial density of smooth muscle cells positive to estrogen receptors between the groups. In contradiction to this, superficial density of smooth muscle cells positive to progesterone receptors was higher in group with PS than in patients without, 343 (±171) and 240 (±123), respectively. The difference was statistically significant (p < 0.05). Conclusion: The amount of cells with sex hormone receptors, not the level of hormones, could play a role in PS pathology. Our results show that progesterone is more important than estrogen in effector organs.
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Dou, Mengmeng, Keyan Zhu, Zhirui Fan, Yuxuan Zhang, Xiufang Chen, Xueliang Zhou, Xianfei Ding, et al. "Reproductive Hormones and Their Receptors May Affect Lung Cancer." Cellular Physiology and Biochemistry 44, no. 4 (2017): 1425–34. http://dx.doi.org/10.1159/000485538.
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Background/Aims: In contrast to men, women have experienced a rapid increase in lung cancer mortality. Numerous studies have found that the sex differences in lung cancer are due to reproductive hormones. Experiments in female mice with and without ovariectomy were performed to explore the possible mechanism by which sex hormones (and their receptors) influence lung cancer. Methods: Twenty-four female C57BL/6 mice aged 56-62 days were randomly divided into the ovariectomized group and the control group. In the ovariectomized group, the bilateral ovaries were removed via the dorsal approach, while the control group underwent a sham operation with bilateral ovarian fat resection at the same sites. After 3 weeks of recovery, Lewis lung cancer cells were transplanted into these mice by subcutaneous inoculation of a tumour cell suspension to establish the ovariectomized lung cancer model. Beginning on the 6th day after subcutaneous inoculation, mouse weight and transplanted tumour volume were measured every 3 days. After 3 weeks, all the mice were killed by cervical dislocation, and we measured the tumour weight. Mouse serum and tumour tissues were removed. Then, the serum levels of E2 (oestradiol) and T (testosterone) were detected by ELISA; the protein expression levels of AR (androgen receptor), ERα (oestrogen receptor α) and ERβ (oestrogen receptor β) were detected by Western Blot and IHC (immunohistochemistry); and the mRNA expression levels of AR, ERα and ERβ were detected by qRT-PCR (quantitative real-time polymerase chain reaction) in the ovariectomized and control groups. Results: Compared with the control group, both mouse weight and transplanted tumour volume increased rapidly in the ovariectomized group, and the transplanted tumour weight was significantly heavier in the ovariectomized group (1.83±0.40 and 3.13±0.43, P<0.05). E2 and T serum levels decreased exponentially in the ovariectomized group, while the E2/T ratio increased compared with the control group (E2: 55.88±11.45 and 78.21±9.37; T: 0.82±0.14 and 1.46±0.16; ratio: 69.62±14.43±29.81 and 52.22±5.42; all P<0.05). The Western blot and IHC results indicated that AR, ERα and ERβ protein expression levels were obviously higher in transplanted tumour and lung tissues from the ovariectomized group, with particular increases in ERβ in transplanted tumour tissue and in ERα in lung tissue. The PCR results also showed markedly higher mRNA expression levels of AR, ERα and ERβ in the ovariectomized group, and in particular, ERβ in transplanted tumour tissue and ERα in lung tissue were significantly increased in the ovariectomized group. Conclusion: Ovariectomy decreased E2 and T serum levels and increased the E2/T ratio in mice, and this imbalance in the internal environment promoted the growth of transplanted tumours. Sex hormone disorder not only promoted transplanted tumour growth but also significantly reduced the protein and mRNA expression levels of sex hormone receptors. The metabolism of E2 and T may affect the growth, proliferation and metabolism of lung cancer cells, and the mechanism by which sex hormones and their receptors influence lung cancer is worthy of further research.
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Honda, Shozo, Phillipe Loher, Megumi Shigematsu, Juan P. Palazzo, Ryusuke Suzuki, Issei Imoto, Isidore Rigoutsos, and Yohei Kirino. "Sex hormone-dependent tRNA halves enhance cell proliferation in breast and prostate cancers." Proceedings of the National Academy of Sciences 112, no. 29 (June 29, 2015): E3816—E3825. http://dx.doi.org/10.1073/pnas.1510077112.
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Sex hormones and their receptors play critical roles in the development and progression of the breast and prostate cancers. Here we report that a novel type of transfer RNA (tRNA)-derived small RNA, termed Sex HOrmone-dependent TRNA-derived RNAs (SHOT-RNAs), are specifically and abundantly expressed in estrogen receptor (ER)-positive breast cancer and androgen receptor (AR)-positive prostate cancer cell lines. SHOT-RNAs are not abundantly present in ER− breast cancer, AR− prostate cancer, or other examined cancer cell lines from other tissues. ER-dependent accumulation of SHOT-RNAs is not limited to a cell culture system, but it also occurs in luminal-type breast cancer patient tissues. SHOT-RNAs are produced from aminoacylated mature tRNAs by angiogenin-mediated anticodon cleavage, which is promoted by sex hormones and their receptors. Resultant 5′- and 3′-SHOT-RNAs, corresponding to 5′- and 3′-tRNA halves, bear a cyclic phosphate (cP) and an amino acid at the 3′-end, respectively. By devising a “cP-RNA-seq” method that is able to exclusively amplify and sequence cP-containing RNAs, we identified the complete repertoire of 5′-SHOT-RNAs. Furthermore, 5′-SHOT-RNA, but not 3′-SHOT-RNA, has significant functional involvement in cell proliferation. These results have unveiled a novel tRNA-engaged pathway in tumorigenesis of hormone-dependent cancers and implicate SHOT-RNAs as potential candidates for biomarkers and therapeutic targets.
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Amenyogbe, Eric, Gang Chen, Zhongliang Wang, Xiaoying Lu, Mingde Lin, and Ai Ying Lin. "A Review on Sex Steroid Hormone Estrogen Receptors in Mammals and Fish." International Journal of Endocrinology 2020 (February 7, 2020): 1–9. http://dx.doi.org/10.1155/2020/5386193.
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Steroid hormones play essential roles in the reproductive biology of vertebrates. Estrogen exercises its effect through estrogen receptors and is not only a female reproductive hormone but acts virtually in all vertebrates, including fish, and is involved in the physiological and pathological states in all males and females. Estrogen has been implicated in mandible conservation and circulatory and central nervous systems as well as the reproductive system. This review intended to understand the structure, function, binding affinities, and activations of estrogens and estrogen receptors and to discuss the understanding of the role of sex steroid hormone estrogen receptors in mammals and fish.
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McEwan, Iain J. "Sex, drugs and gene expression: signalling by members of the nuclear receptor superfamily." Essays in Biochemistry 40 (June 1, 2004): 1–10. http://dx.doi.org/10.1042/bse0400001.
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It is almost 20 years since the first steroid receptor cDNAs were cloned, a development that led to the concept of a superfamily of ligand-activated transcription factors: the nuclear receptors. Natural ligands for nuclear receptors are generally lipophilic in nature and include steroid hormones, bile acids, fatty acids, thyroid hormones, certain vitamins and prostaglandins. Nuclear receptors act principally to directly control patterns of gene expression and play vital roles during development and in the regulation of metabolic and reproductive functions in the adult organism. Since the original cloning experiments, considerable progress has been made in our understanding of the structure, mechanisms of action and biology of this important family of proteins.
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Chang, Ya-Ting, Yung-Lung Chen, and Hong-Yo Kang. "Revealing the Influences of Sex Hormones and Sex Differences in Atrial Fibrillation and Vascular Cognitive Impairment." International Journal of Molecular Sciences 22, no. 16 (August 16, 2021): 8776. http://dx.doi.org/10.3390/ijms22168776.
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The impacts of sex differences on the biology of various organ systems and the influences of sex hormones on modulating health and disease have become increasingly relevant in clinical and biomedical research. A growing body of evidence has recently suggested fundamental sex differences in cardiovascular and cognitive function, including anatomy, pathophysiology, incidence and age of disease onset, symptoms affecting disease diagnosis, disease severity, progression, and treatment responses and outcomes. Atrial fibrillation (AF) is currently recognized as the most prevalent sustained arrhythmia and might contribute to the pathogenesis and progression of vascular cognitive impairment (VCI), including a range of cognitive deficits, from mild cognitive impairment to dementia. In this review, we describe sex-based differences and sex hormone functions in the physiology of the brain and vasculature and the pathophysiology of disorders therein, with special emphasis on AF and VCI. Deciphering how sex hormones and their receptor signaling (estrogen and androgen receptors) potentially impact on sex differences could help to reveal disease links between AF and VCI and identify therapeutic targets that may lead to potentially novel therapeutic interventions early in the disease course of AF and VCI.
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Brun, Claire, Jean-Marie Exbrayat, and Michel Raquet. "Localization of Receptors for Sex Steroids and Pituitary Hormones in the Female Genital Duct throughout the Reproductive Cycle of a Viviparous Gymnophiona Amphibian, Typhlonectes compressicauda." Animals 11, no. 1 (December 22, 2020): 2. http://dx.doi.org/10.3390/ani11010002.
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Reproduction in vertebrates is controlled by the hypothalamo-pituitary-gonadal axis, and both the sex steroid and pituitary hormones play a pivotal role in the regulation of the physiology of the oviduct and events occurring within the oviduct. Their hormonal actions are mediated through interaction with specific receptors. Our aim was to locate α and β estrogen receptors, progesterone receptors, gonadotropin and prolactin receptors in the tissues of the oviduct of Typhlonectes compressicauda (Amphibia, Gymnophiona), in order to study the correlation between the morphological changes of the genital tract and the ovarian cycle. Immunohistochemical methods were used. We observed that sex steroids and pituitary hormones were involved in the morpho-functional regulation of oviduct, and that their cellular detection was dependent on the period of the reproductive cycle.
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Fuentes, Nathalie, and Patricia Silveyra. "Endocrine regulation of lung disease and inflammation." Experimental Biology and Medicine 243, no. 17-18 (December 2018): 1313–22. http://dx.doi.org/10.1177/1535370218816653.
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Sex-based disparities have been identified in respiratory physiology, and in many chronic lung diseases including asthma, chronic obstructive pulmonary disease, and cystic fibrosis. The observed sex differences in lung disease prevalence and incidence have been linked to changes in circulating levels of sex hormones that start after puberty and that have been shown to affect physiological and immunological functions. While the exact roles of male and female sex hormones in these processes have not been fully elucidated, it is now evident that these can target many lung cell types and affect several functions of the respiratory system. In this mini-review, we have summarized seminal studies aimed to understand the effects of the most relevant male and female sex hormones (estrogens, progesterone, and androgens) and their receptors on lung function. Moreover, we have reviewed the known influences of sex hormones and of the hypothalamic–pituitary–gonadal axis in lung disease and immunity. Understanding the roles of sex hormones in the regulation of lung function and inflammation is the first step for the potential development of more effective therapeutic options to prevent and treat lung disease in men and women. Impact statement Sex-differences in the incidence and severity of inflammatory lung diseases have been recognized for years. Women of reproductive age are more likely to suffer from chronic lung disease, with higher mortality rates than men. Physiological changes in hormone levels such as those occurring during the menstrual cycle, pregnancy, and menopause have been associated with lung function changes and asthma symptoms. Despite this, the roles of sex hormones in the mechanisms associated with lung diseases have not been fully elucidated. This review summarizes basic and clinical studies of sex hormones as potential modulators of lung function and inflammation. The information obtained from sex-specific research on lung physiology and pathology will potentially help in the development of sex-specific therapeutics for inflammatory lung disease that may account for the hormonal status of the patient.
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Celayir, Sinan. "Is there a `bladder sex'? The relation of different sex hormones and sex hormone receptors in bladder in childhood." Medical Hypotheses 59, no. 2 (August 2002): 186–90. http://dx.doi.org/10.1016/s0306-9877(02)00245-1.
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Dahir, Naima S., Ashley N. Calder, Blake J. McKinley, Yan Liu, and Timothy A. Gilbertson. "Sex differences in fat taste responsiveness are modulated by estradiol." American Journal of Physiology-Endocrinology and Metabolism 320, no. 3 (March 1, 2021): E566—E580. http://dx.doi.org/10.1152/ajpendo.00331.2020.
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Using molecular, cellular, and behavioral analyses, this study shows that sex differences occur in fat taste in a mouse model. Female mice are more responsive to fatty acids, leading to an overall decrease in intake and fatty acid preference. These differences are linked to sex hormones, as estradiol enhances taste cell responsiveness to fatty acids during periods of low circulating estrogen following ovariectomy and in males. Estradiol is ineffective in altering fatty acid signaling during a high-estrogen period and in ovariectomized mice on hormone replacement. Thus, taste receptor cells are a direct target for actions of estrogen, and there are multiple receptors with differing patterns of expression in taste cells.
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Vermeirsch, Hilde, Wim Van Den Broeck, and Paul Simoens. "Immunolocalization of sex steroid hormone receptors in canine vaginal and vulvar tissue and their relation to sex steroid hormone levels." Reproduction, Fertility and Development 14, no. 4 (2002): 251. http://dx.doi.org/10.1071/rd01088.
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The aim of this immunohistochemical study was to describe the cellular distribution of the estrogen receptor-α (ERα), progesterone receptor (PR) and androgen receptor (AR) in canine vaginal and vulvar tissue. Samples were taken from dogs in different stages of the estrous cycle. Nuclear staining for ERα, PR and AR was observed in surface epithelium, stromal and smooth muscle cells. Receptors were also expressed in vulvar skin. Cytoplasmic staining for AR was observed in basal and parabasal cell layers of vulvar and vaginal epithelium. For all three receptors, staining intensity was generally higher in stromal cells compared with epithelial cells, suggesting that stromal cells may be more receptive to steroid hormone action. Therefore, as in other tissues of the female genital tract, stromal-epithelial interactions induced by sex steroid hormones may be of importance in canine vaginal and vulvar tissues. No cyclic changes in receptor immunostaining were observed. Significant positive correlations were found between receptor immunostaining in some vaginal and vulvar cell groups and the serum concentrations of estradiol-17β and testosterone, but not with the serum progesterone concentration. Significant negative correlations were found between ERα immunostaining in epithelial and stromal cells of the vagina and the serum estradiol-17α concentration, suggesting a negative feedback mechanism between estradiol-17β and its receptor. Both cell types play a role in the differentiation of vaginal epithelium, under the influence of estradiol-17β
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Luo, Sheng-Dean, Tai-Jan Chiu, Wei-Chih Chen, and Ching-Shuen Wang. "Sex Differences in Otolaryngology: Focus on the Emerging Role of Estrogens in Inflammatory and Pro-Resolving Responses." International Journal of Molecular Sciences 22, no. 16 (August 16, 2021): 8768. http://dx.doi.org/10.3390/ijms22168768.
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Otolaryngology (also known as ear, nose, and throat (ENT)) diseases can be significantly affected by the level of sex hormones, which indicates that sex differences affect the manifestation, pathophysiology, and outcomes of these diseases. Recently, increasing evidence has suggested that proinflammatory responses in ENT diseases are linked to the level of sex hormones. The sex hormone receptors are present on a wide variety of immune cells; therefore, it is evident that they play crucial roles in regulating the immune system and hence affect the disease progression of ENT diseases. In this review, we focus on how sex hormones, particularly estrogens, regulate ENT diseases, such as chronic rhinosinusitis, vocal fold polyps, thyroid cancer, Sjögren’s syndrome, and head and neck cancers, from the perspectives of inflammatory responses and specialized proresolving mediator-driven resolution. This paper aims to clarify why considering sex differences in the field of basic and medical research on otolaryngology is a key component to successful therapy for both males and females in the future.
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Mierzejewska, Kasia, Ewa Suszynska, Sylwia Borkowska, Malwina Suszynska, Maja Maj, Janina Ratajczak, Magdalena Kucia, and Mariusz Z. Ratajczak. "Novel In Vivo Evidence That Not Only Androgens But Also Pituitary Gonadotropins and Prolactin Directly Stimulate Murine Bone Marrow Stem Cells – Implications For Potential Treatment Strategies In Aplastic Anemias." Blood 122, no. 21 (November 15, 2013): 2476. http://dx.doi.org/10.1182/blood.v122.21.2476.2476.
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Abstract Background Hematopoietic stem/progenitor cells (HSPCs) are exposed in vivo to several growth factors, cytokines, chemokines, and bioactive lipids in bone marrow (BM) in addition to various sex hormones circulating in peripheral blood (PB). It is known that androgen hormones (e.g., danazol) is employed in the clinic to treat aplastic anemia patients. However, the exact mechanism of action of sex hormones secreted by the pituitary gland or gonads is not well understood. Therefore, we performed a complex series of experiments to address the influence of pregnant mare serum gonadotropin (PMSG), luteinizing hormone (LH), follicle-stimulating hormone (FSH), androgen (danazol) and prolactin (PRL) on murine hematopoiesis. In particular, from a mechanistic view we were interested in whether this effect depends on stimulation of BM-residing stem cells or is mediated through the BM microenvironment. Materials and Methods To address this issue, normal 2-month-old C57Bl6 mice were exposed or not to daily injections of PMSG (10 IU/mice/10 days), LH (5 IU/mice/10 days), FSH (5 IU/mice/10 days), danazol (4 mg/kg/10 days) and PRL (1 mg/day/5days). Subsequently, we evaluated changes in the BM number of Sca-1+Lin–CD45– that are precursors of long term repopulating hematopoietic stem cells (LT-HSCs) (Leukemia 2011;25:1278–1285) and bone forming mesenchymal stem cells (Stem Cell & Dev. 2013;22:622-30) and Sca-1+Lin–CD45+ hematopoietic stem/progenitor cells (HSPC) cells by FACS, the number of clonogenic progenitors from all hematopoietic lineages, and changes in peripheral blood (PB) counts. In some of the experiments, mice were exposed to bromodeoxyuridine (BrdU) to evaluate whether sex hormones affect stem cell cycling. By employing RT-PCR, we also evaluated the expression of cell-surface and intracellular receptors for hormones in purified populations of murine BM stem cells. In parallel, we studied whether stimulation by sex hormones activates major signaling pathways (MAPKp42/44 and AKT) in HSPCs and evaluated the effect of sex hormones on the clonogenic potential of murine CFU-Mix, BFU-E, CFU-GM, and CFU-Meg in vitro. We also sublethally irradiated mice and studied whether administration of sex hormones accelerates recovery of peripheral blood parameters. Finally, we determined the influence of sex hormones on the motility of stem cells in direct chemotaxis assays as well as in direct in vivo stem cell mobilization studies. Results We found that 10-day administration of each of the sex hormones evaluated in this study directly stimulated expansion of HSPCs in BM, as measured by an increase in the number of these cells in BM (∼2–3x), and enhanced BrdU incorporation (the percentage of quiescent BrdU+Sca-1+Lin–CD45– cells increased from ∼2% to ∼15–35% and the percentage of BrdU+Sca-1+Lin–CD45+ cells increased from 24% to 43–58%, Figure 1). These increases paralleled an increase in the number of clonogenic progenitors in BM (∼2–3x). We also observed that murine Sca-1+Lin–CD45– and Sca-1+Lin–CD45+ cells express sex hormone receptors and respond by phosphorylation of MAPKp42/44 and AKT in response to exposure to PSMG, LH, FSH, danazol and PRL. We also observed that administration of sex hormones accelerated the recovery of PB cell counts in sublethally irradiated mice and slightly mobilized HSPCs into PB. Finally, in direct in vitro clonogenic experiments on purified murine SKL cells, we observed a stimulatory effect of sex hormones on clonogenic potential in the order: CFU-Mix > BFU-E > CFU-Meg > CFU-GM. Conclusions Our data indicate for the first time that not only danazol but also several pituitary-secreted sex hormones directly stimulate the expansion of stem cells in BM. This effect seems to be direct, as precursors of LT-HSCs and HSPCs express all the receptors for these hormones and respond to stimulation by phosphorylation of intracellular pathways involved in cell proliferation. These hormones also directly stimulated in vitro proliferation of purified HSPCs. In conclusion, our studies support the possibility that not only danazol but also several other upstream pituitary sex hormones could be employed to treat aplastic disorders and irradiation syndromes. Further dose- and time-optimizing mouse studies and studies with human cells are in progress in our laboratories. Disclosures: No relevant conflicts of interest to declare.
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Liu, RenHui, Xue Kang, LiPing Xu, HongLei Nian, XinWei Yang, HaoTian Shi, and XiuJuan Wang. "Effect of the Combined Extracts of Herba Epimedii and Fructus Ligustri Lucidi on Sex Hormone Functional Levels in Osteoporosis Rats." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/184802.
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The combination of Herba Epimedii and Fructus Ligustri Lucidi has been used to treat osteoporosis for almost 50 years by Professor Shizeng Li, a famous doctor of traditional Chinese medicine (TCM). However, it is unclear whether the combination of the effective constituents of the two herbs may have a protective influence on the skeleton. In the present study, we investigated the effects of the combination extracts of Herba Epimedii and Fructus Ligustri Lucidi on rat model of osteoporosis induced by retinoic acid by gavage. With administrations of the combination extracts of the two herbs (50, 100, and 200 mg/kg/day) via oral gavage for 3 weeks, bone mineral density (BMD), femur histomorphometry, some sex hormones, and sex hormone receptors were measured. Results showed that the combined extracts could increase BMD, affect bone histomorphometry, coordinate the sex hormones at the level of hypothalamus-pituitary-gonad axis, and increase the protein and mRNA expressions of sex hormone receptors. The findings suggested that the combination extracts of Herba Epimedii and Fructus Ligustri Lucidi might be beneficial as an alternative medicine for the prevention and treatment of osteoporosis.
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Nasser, Suzanne A., Elham A. Afify, Firas Kobeissy, Bassam Hamam, Ali H. Eid, and Mahmoud M. El-Mas. "Inflammatory Basis of Atherosclerosis: Modulation by Sex Hormones." Current Pharmaceutical Design 27, no. 18 (June 24, 2021): 2099–111. http://dx.doi.org/10.2174/1381612827666210122142811.
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Atherosclerosis-related cardiovascular diseases (CVDs) are the leading cause of death globally. Several lines of evidence are supportive of the contributory role of vascular inflammation in atherosclerosis. Diverse immune cell types, including monocytes/macrophages, T-cells and neutrophils, as well as specialized proresolving lipid mediators, have been successfully characterized as key players in vascular inflammation. The increased prevalence of atherosclerotic CVD in men in comparison to age-matched premenopausal women and the abolition of sex differences in prevalence during menopause strongly suggest a pivotal role of sex hormones in the development of CVD. Indeed, many animal and human studies conclusively implicate sex hormones as a crucial component in driving the immune response. This is further corroborated by the effective identification of sex hormone receptors in vascular endothelial cells, vascular smooth muscle cells and immune cells. Collectively, these findings suggest a cellular communication between sex hormones and vascular or immune cells underlying the vascular inflammation in atherosclerosis. The aim of this review is to provide an overview of vascular inflammation as a causal cue underlying atherosclerotic CVDs within the context of the modulatory effects of sex hormones. Moreover, the cellular and molecular signaling pathways underlying the sex hormones- immune system interactions as potential culprits for vascular inflammation are highlighted with detailed and critical discussion. Finally, the review concludes by speculations on the potential sex-related efficacy of currently available immunotherapies in mitigating vascular inflammation. Conceivably, a deeper understanding of the immunoregulatory influence of sex hormones on vascular inflammation-mediated atherosclerosis permits sex-based management of atherosclerosis-related CVDs.
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Babichev, V. N., Ye L. Adamskaya, and T. A. Peryshkova. "Analysis of hypothalamo-hypophyseo-gonadal relationships in female rats with experimental diabetes." Problems of Endocrinology 40, no. 1 (February 15, 1994): 46–50. http://dx.doi.org/10.14341/probl11334.
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Hypothalamo-hypophyseo-gonadal system functional activity was studied in rats with streptozotocin diabetes. In intact rats concentrations of sex hormones nuclear receptors were measured in the hypothalamic preopticoanterior, mediobasal segments and in the adenohypophysis, as were blood serum gonadotropins and sex hormones. Estradiol and progesterone were injected to ovariectomized females and LH-RH levels measured in preopticoanterior segment of the hypothalamus, arcuate nucleus, and median eminence, as well as LH and FSH concentrations in the blood in order to detect disorders in basal and cyclic gonadotropin secretion. Streptozotocin injection to cycling females disordered the estral cycle and was associated with reduction of LH, FSH, and sex hormones basal and cyclic secretion. Estradiol nuclear receptors concentrations reduced in the preopticoanterior hypothalamus and hypophysis, the count of nuclear testosterone-binding sites reduced only in the hypophysis. Gonadotropin wave stimulated with sex steroids in ovariectomized females was reduced in diabetes because of changed activity of LH-RH-producing system. We believe that changes in basal and cyclic secretion of gonadotropins in rat females with experimental diabetes is explained by reduced activity of LH-RH-producing system and receptor binding at the level of the hypothalamo-hypophyseal complex.
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Nacci, Andrea, Bruno Fattori, Fabio Basolo, Maria E. Filice, Katia De Jeso, Luca Giovannini, Luca Muscatello, Fabio Matteucci, and Francesco Ursino. "Sex Hormone Receptors in Vocal Fold Tissue: A Theory about the Influence of Sex Hormones in the Larynx." Folia Phoniatrica et Logopaedica 63, no. 2 (2011): 77–82. http://dx.doi.org/10.1159/000316136.
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Harvey, Brian J., Steven Condliffe, and Christina M. Doolan. "Sex and Salt Hormones: Rapid Effects in Epithelia." Physiology 16, no. 4 (August 2001): 174–77. http://dx.doi.org/10.1152/physiologyonline.2001.16.4.174.
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Recent evidence points to protein kinase C isoforms as highly specific receptors for aldosterone and estradiol in epithelia. The end targets of the kinase activation are Na+/H+ exchange and K+ and Ca2+ channels. The physiological role of the nongenomic response is to increase electrolyte absorption and inhibit secretion in pluripotential epithelia.