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Mothers and Babies Research Centre, Department of Obstetrics and Gynaecology, University of Newcastle, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia
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Mothers and Babies Research Centre, Department of Obstetrics and Gynaecology, University of Newcastle, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia
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Mothers and Babies Research Centre, Department of Obstetrics and Gynaecology, University of Newcastle, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia
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Mothers and Babies Research Centre, Department of Obstetrics and Gynaecology, University of Newcastle, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia
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Mothers and Babies Research Centre, Department of Obstetrics and Gynaecology, University of Newcastle, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia
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Mothers and Babies Research Centre, Department of Obstetrics and Gynaecology, University of Newcastle, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia
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Mothers and Babies Research Centre, Department of Obstetrics and Gynaecology, University of Newcastle, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia
Mothers and Babies Research Centre, Department of Obstetrics and Gynaecology, University of Newcastle, Hunter Medical Research Institute, New Lambton Heights, New South Wales, Australia
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analysed from term pregnancies not in labour and following labour. Steroid hormones are fundamentally important regulators of gestational tissue function including inflammatory reactions. The responsiveness to these hormones varies between tissues and
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University of Melbourne and Baker HDI Department of Cardiometabolic Health and Disease, Melbourne, Australia
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& Young 2009 ). The MR is a member of the nuclear receptor superfamily of transcription factors and is most closely related to the steroid hormone receptors – glucocorticoid receptor (GR), progesterone receptor, androgen receptor (AR), oestrogen receptor
Geriatric Research, Division of Endocrinology, Division of Gastroenterology and Hepatology, Department of Obstetrics and Gynecology, State Key Laboratory of Cellular Stress Biology, Program in Molecular Medicine, Education and Clinical Center (GRECC-182B), VA Palo Alto Health Care System, 3801 Miranda Avenue, Palo Alto, California 94304, USA
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Geriatric Research, Division of Endocrinology, Division of Gastroenterology and Hepatology, Department of Obstetrics and Gynecology, State Key Laboratory of Cellular Stress Biology, Program in Molecular Medicine, Education and Clinical Center (GRECC-182B), VA Palo Alto Health Care System, 3801 Miranda Avenue, Palo Alto, California 94304, USA
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Geriatric Research, Division of Endocrinology, Division of Gastroenterology and Hepatology, Department of Obstetrics and Gynecology, State Key Laboratory of Cellular Stress Biology, Program in Molecular Medicine, Education and Clinical Center (GRECC-182B), VA Palo Alto Health Care System, 3801 Miranda Avenue, Palo Alto, California 94304, USA
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Geriatric Research, Division of Endocrinology, Division of Gastroenterology and Hepatology, Department of Obstetrics and Gynecology, State Key Laboratory of Cellular Stress Biology, Program in Molecular Medicine, Education and Clinical Center (GRECC-182B), VA Palo Alto Health Care System, 3801 Miranda Avenue, Palo Alto, California 94304, USA
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Introduction Extensive experimental evidence now indicates that aging in humans and animal models is associated with a general decline in steroid hormone production ( Zaidi et al . 2012 ). Similarly, a number of in vitro studies have clearly
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Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, Minnesota, USA
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Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, Minnesota, USA
Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota, USA
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Introduction Of the 48 ligand-activated and ‘orphan’ (i.e. ligands remain unidentified) nuclear receptors (NRs), six are related members of the SR superfamily whose steroid hormone ligands are primarily derived from cholesterol metabolism
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The current and expanded view of transcriptional regulation by the steroid/thyroid superfamily of nuclear transcription factors integrates not only the hormone-dependent but also the hormone-independent cellular signaling mechanisms in physiology and reproduction. This effort has vastly been aided by the identification of steroid hormone receptors as transcriptional mediators of a variety of ligands, whose transcriptional response is dependent upon cross-talk with distinct signal transduction pathways, their recruitment of coregulators, alteration of chromatin structure and identification of specific interactive motifs within the receptors themselves. This review will provide a framework for the current concepts in the field of steroid hormone action as exemplified by our studies on progesterone receptor in female sexual behavior.
Department of Obstetrics and Gynaecology, University of Regensburg, Regensburg, Germany
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Department of Obstetrics and Gynaecology, University of Regensburg, Regensburg, Germany
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Department of Obstetrics and Gynaecology, University of Regensburg, Regensburg, Germany
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Department of Obstetrics and Gynaecology, University of Regensburg, Regensburg, Germany
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Department of Obstetrics and Gynaecology, University of Regensburg, Regensburg, Germany
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Department of Obstetrics and Gynaecology, University of Regensburg, Regensburg, Germany
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Department of Obstetrics and Gynaecology, University of Regensburg, Regensburg, Germany
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Department of Obstetrics and Gynaecology, University of Regensburg, Regensburg, Germany
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gonadotropin-releasing hormone-induced biphasic luteinizing hormone secretory responses and inositol phosphate accumulation in rat anterior pituitary cells and alpha T3-1 gonadotrophs. Journal of Steroid Biochemistry and Molecular Biology 54 101 –109
Tianjin Key Laboratory for Prevention and Control of Occupational and Environmental Hazard, Department of Pathogenic Biology and Immunology, Department of Infectious Diseases, Department of Pharmacology, Department of Gynecology and Obstetrics, Tianjin, People's Republic of China
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, Rabinovich et al . 2007 , Yang et al . 2009 , Wang et al . 2010 a , 2012 ). Recently, the results of our studies indicated that IL6 secreted by OVCA cells may contribute to the refractoriness of these cells to TAM via ER isoforms and steroid hormone
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Steroid hormones synthesized from cholesterol in the adrenal gland are important regulators of many physiological processes. It is now well documented that the expression of many genes required for steroid biosynthesis is dependent on the coordinated expression of the nuclear receptor steroidogenic factor-1 (SF-1). However, transcriptional mechanisms underlying the species-specific, developmentally programmed and hormone-dependent modulation of the adrenal steroid pathways remain to be elucidated. Recently, we demonstrated that the transcriptional regulating protein of 132 kDa (TReP-132) acts as a coactivator of SF-1 to regulate human P450scc gene transcription in human adrenal NCI-H295 cells. The present study shows that overexpression of TReP-132 increases the level of active steroids produced in NCI-H295 cells. The conversion of pregnenolone to downstream steroids following TReP-132 expression showed increased levels of glucocorticoids, C(19) steroids and estrogens. Correlating with these data, TReP-132 increases P450c17 activities via the induction of transcript levels and promoter activity of the P450c17 gene, an effect that is enhanced in the presence of cAMP or SF-1. In addition, P450aro activity and mRNA levels are highly induced by TReP-132, whereas 3beta-hydroxysteroid dehydrogenase type II and P450c11aldo transcript levels are only slightly modulated. Taken together, these results demonstrate that TReP-132 is a trans-acting factor of genes involved in adrenal glucocorticoid, C(19) steroid and estrogen production.
Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Department of Obstetrics and Gynecology, Tufts–New England Medical Center, Boston, MA 02111, USA
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Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Department of Obstetrics and Gynecology, Tufts–New England Medical Center, Boston, MA 02111, USA
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Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Department of Obstetrics and Gynecology, Tufts–New England Medical Center, Boston, MA 02111, USA
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Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Department of Obstetrics and Gynecology, Tufts–New England Medical Center, Boston, MA 02111, USA
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Introduction The gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), are critical modulators of sexual development and reproductive function, acting on the gonads to stimulate both steroidogenesis and
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Apolipoprotein AI (apo AI) is the major protein component of the serum high-density lipoprotein (HDL) particles. The antiatherogenic properties of apo AI alone or as part of HDL and their inverse correlation with the incidence of coronary heart disease underlie the clinical importance of the protein. A detailed understanding of the mechanisms by which apo AI is regulated will help us develop new and better ways to manipulate expression of the protein. Although there are many factors that influence apo AI expression, endogenous hormones are attractive because simple changes in abundance of these compounds will alter gene activity. Hormones belonging to the thyroid/steroid family that influence activity of the gene include thyroid hormone, glucocorticoids, gender-specific steroids and retinoic acid. Whereas thyroid, glucocorticoid and estradiol enhance activity of the gene, retinoic acid and androgens decrease it. The mechanisms that mediate the effects of the hormones include direct effects of the ligand and nuclear receptor complex on gene activity. However, indirect means involving the participation of transcription factors other than the hormone receptors are also possible. In summary, members of the same hormone family may have different mechanisms that mediate their activities on apo AI gene activity.
