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The placenta regulates materno-fetal nutrient transfer and secretes hormones that enable maternal physiological support of the pregnancy. In mice, these functions are performed by the labyrinth (Lz) and junctional (Jz) zones, respectively. Insulin-like growth factor 2 (Igf2) is an imprinted gene expressed by the conceptus that is important for promoting fetal growth and placenta formation. However, the specific role of Igf2 in the Jz in regulating placental endocrine function and fetal development is unknown. This study used a novel model to investigate the effect of conditional loss of Igf2 in the Jz (Jz-Igf2UE) on placental endocrine cell formation and the expression of hormones and IGF signaling components in placentas from female and male fetuses. Jz-Igf2UE altered gross placental structure and expression of key endocrine and signaling genes in a sexually dimorphic manner. The volumes of spongiotrophoblast and glycogen trophoblast in the Jz were decreased in placentas from female but not male fetuses. Expression of insulin receptor was increased and expression of the MAPK pathway genes (Mek1, P38α) decreased in the placental Jz of female but not male fetuses. In contrast, expression of the type-1 and -2 IGF receptors and the MAPK pathway genes (H-ras, N-ras, K-ras) was decreased in the placental Jz from male but not female fetuses. Expression of the steroidogenic gene, Cyp17a1, was increased and placental lactogen-2 was decreased in the placenta of both sexes. In summary, we report that Jz-Igf2UE alters the cellular composition, IGF signaling components and hormone expression of the placental Jz in a manner largely dependent on fetal sex.
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The Florey Institute of Neuroscience and Mental Health, Microscopy Facility, Melbourne, Victoria, Australia
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Barwon Health Laboratory, Barwon Health, University Hospital, Geelong, Victoria, Australia
Institute for Physical and Mental Health and Clinical Transformation, School of Medicine, Deakin University, Geelong, Victoria, Australia
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ARC Centre of Excellence for Nanoscale Biophotonics, RMIT University, Melbourne, Victoria, Australia
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neonatal nutrition causes perturbations in hypothalamic neural circuits controlling reproductive function . Journal of Neuroscience 32 11486 – 11494 . ( https://doi.org/10.1523/JNEUROSCI.6074-11.2012 ) 10.1523/JNEUROSCI.6074-11.2012 Chan KA Jazwiec
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School of Literature, Science, and Arts, University of Michigan, Ann Arbor, Michigan, USA
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Neuroscience Graduate Program, University of Michigan, Ann Arbor, Michigan, USA
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Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas and Facultad de Ciencias Exactas y Naturales, Universidad de Buenos, Buenos Aires, Argentina
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2018a Leptin and brain-adipose crosstalks . Nature Reviews: Neuroscience 19 153 – 165 . ( https://doi.org/10.1038/nrn.2018.7 ) Caron A Dungan Lemko HM Castorena CM Fujikawa T Lee S Lord CC Ahmed N Lee CE Holland WL Liu C
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The Ritchie Centre, Hudson Institute of Medical Research, Clayton, Australia
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Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, UK
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hypothalamic-pituitary-adrenal axis: development, programming actions of hormones and maternal-fetal interactions . Frontiers in Behavioral Neuroscience 14 601939 . ( https://doi.org/10.3389/fnbeh.2020.601939 ) Sloboda DM Moss TJM Gurrin LC Challis
Department of Biotechnology, Genetics, and Cellular Biology, State University of Maringá, Maringá, Parana, Brazil
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Miranda RA Palma-Rigo K , 2018 Treatment with soy isoflavones during early adulthood improves metabolism in early postnatally overfed rats . Nutritional Neuroscience 21 25 – 32 . ( https://doi.org/10.1080/1028415X.2016.1213007 ) Talaei M
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In heterologous expression systems, human GnRH receptors (hGnRHRs) are poorly expressed at the cell surface and this may reflect inefficient exit from the endoplasmic reticulum. Here, we have defined the proportion of GnRHRs at the cell surface using a novel assay based on adenoviral transduction with epitope-tagged GnRHRs followed by staining and semi-automated imaging. We find that in MCF7 (breast cancer) cells, the proportional cell surface expression (PCSE) of hGnRHRs is remarkably low (<1%), when compared with Xenopus laevis (X) GnRHRs (∼40%). This distinction is retained at comparable whole cell expression levels, and the hGnRHR PCSE is increased by addition of the XGnRHR C-tail (h.XGnRHR) or by a membrane-permeant pharmacological chaperone (IN3). The IN3 effect is concentration- and time-dependent and IN3 also enhances the hGnRHR-mediated (but not h.XGnRHR- or mouse GnRHR-mediated) stimulation of [3H]inositol phosphate accumulation and the hGnRHR-mediated reduction in cell number. We also find that the PCSE for hGnRHRs and h.XGnRHRs is low and is greatly increased by IN3 in two hormone-dependent cancer lines, but is higher and less sensitive to IN3 in a gonadotrope line. Finally, we show that the effect of IN3 on hGnRHR PCSE is not mimicked or blocked by two peptide antagonists although they do increase the PCSE for h.XGnRHRs, revealing that an antagonist-occupied cell surface GnRHR conformation can differ from that of the unoccupied receptor. The low PCSE of hGnRHRs and this novel peptide antagonist effect may be important for understanding GnRHR function in extrapituitary sites.
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Fetal glucocorticoids have an important role in the pre-partum maturation of physiological systems essential for neonatal survival such as glucogenesis. Consequently, in clinical practice, synthetic glucocorticoids, like dexamethasone, are given routinely to pregnant women threatened with pre-term delivery to improve the viability of their infants. However, little is known about the effects of maternal dexamethasone treatment on the glucogenic capacity of either the fetus or mother. This study investigated the effects of dexamethasone treatment using a clinically relevant dose and regime on glycogen deposition and the activities of glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) in the liver and kidney of pregnant ewes and their fetuses, and of non-pregnant ewes. Dexamethasone administration increased the glycogen content of both the fetal and adult liver within 36 h of beginning treatment. It also increased G6Pase activity in the liver and kidney of the fetuses but not of their mothers or the non-pregnant ewes. Neither hepatic nor renal PEPCK activity was affected by dexamethasone in any group of animals. These changes in glycogen content and G6Pase activity were accompanied by rises in the plasma glucose and insulin concentrations and by a fall in the plasma cortisol level in the fetus and both groups of adult animals. In addition, dexamethasone treatment raised fetal plasma tri-iodothyronine (T3) concentrations and reduced maternal levels of plasma T3 and thyroxine, but had no effect on thyroid hormone concentrations in the non-pregnant ewes. These findings show that maternal dexamethasone treatment increases the glucogenic capacity of both the mother and fetus and has major implications for glucose availability both before and after birth.
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Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, Michigan, USA
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Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia, USA
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Bosch OJ Miklos S Torner L Wales L Waldherr M & Neumann ID 2008 Oxytocin reduces anxiety via ERK1/2 activation: local effect within the rat hypothalamic paraventricular nucleus . European Journal of Neuroscience 27 1947 – 1956 . ( https
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Scheer FAJL Perusquía M Centurion D Buijs RM 2014 The suprachiasmatic nucleus is part of a neural feedback circuit adapting blood pressure response . Neuroscience 266 197 – 207 . ( https://doi.org/10.1016/j.neuroscience.2014.02.018 ) 24583038 10
Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Department of Vascular Medicine, Amsterdam Diabetes Centre, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
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Hypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Amsterdam, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Centre, Leiden, The Netherlands
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Kalsbeek A Soeters MR Eggink HM 2017 Bile acid signaling pathways from the enterohepatic circulation to the central nervous system . Frontiers in Neuroscience 11 617 . 10.3389/fnins.2017.00617 29163019 Naqvi SH Nicholas HJ 1970 Conversion
