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The Placenta and Human Developmental Programming
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  • Cited by 7
  • Edited by Graham J. Burton, Department of Anatomy, University of Cambridge , David J. P. Barker, MRC Epidemiology Resource Centre, University of Southampton , Ashley Moffett, Department of Pathology, University of Cambridge , Kent Thornburg, Department of Obstetrics and Gynecology, Oregon Health and Sciences University, Portland, OR
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Book description

Developmental programming is a rapidly advancing discipline of great importance to basic scientists and health professionals alike. This text integrates, for the first time, contributions from world experts to explore the role of the placenta in developmental programming. The book considers the materno-fetal supply line, and how perturbations of placental development impact on its functional capacity. Chapters examine ways in which environmental, immunological and vascular insults regulate expression of conventional and imprinted genes, along with their impact on placental shape and size, transport, metabolism and endocrine function. Research in animal models is integrated with human clinical and epidemiological data, and questions for future research are identified. Transcripts of discussions between the authors allow readers to engage with controversial issues. Essential reading for researchers in placental biology and developmental programming, as well as specialists and trainees in the wider field of reproductive medicine.

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Contents

  • 9 - The role of the maternal immune response in fetal programming
    pp 102-113
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    Summary

    This introduction provides an overview of the concepts discussed in the book The Placenta and Human Developmental Programming. Developmental programming of the fetus is a phenomenon that has profound implications for the health of individuals and societies. This book explores the current knowledge of the ways in which various aspects of placental development and function may influence fetal programming, and aims to promote further scientific research in their respective fields. The development of the placenta is not autonomous, but is clearly heavily influenced by the uterine mucosa with which the trophoblast interacts. Assessment of placental function in vivo is obviously important for clinical diagnosis and monitoring. The capacity of the placenta to supply adequate nutrients to the fetus is obviously of central importance to the role of the organ in developmental programming, but other aspects of placental function may also operate.
  • 10 - Clinical causes and aspects of placental insufficiency
    pp 114-125
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    Summary

    This chapter uses new epidemiological data to examine the role of materno-placental interactions in initiating chronic disease in the offspring. The size, weight and shape of the placenta are all subject to wide variations. Its size reflects its ability to transfer nutrients. In humans, placental growth responds to maternal influences. Maternal anemia and high maternal body mass index are associated with a high placental weight to birth weight ratio. The observations on hypertension established that the relation between placental size/shape and fetal programming depend on the mother. There are similar materno-placental interactions in the programming of coronary heart disease. Growth of the placental surface is polarized from the time of implantation. The human fetus may attempt to compensate for undernutrition by expansion of the placental surface along its minor axis. The maternal/ placental programming of chronic disease differs in boys and girls.
  • 12 - Placental amino acid transporters
    pp 147-160
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    Summary

    The state of stress may be produced in the body by many causes, but the hypothalamopituitary-adrenal (HPA) axis plays a central coordinating role in the response to both internal and external stressors, substantially mediated through the release of corticotrophin-releasing hormone (CRH) and arginine-vasopressin (AVP). At every stage healthy development presumes the ready availability of a suitable mix of nutrients to support the current needs for cellular growth, elaboration, maturation, function and replication. Placental function plays a critical determining role in the process of fetal programming and the determination of the fetal phenotype. The changes in growth are associated with long-term alterations in behaviour, circulating levels of glucocorticoids and the set of the HPA axis in the offspring. Prepregnancy obesity is increasingly common, and despite the reality of obesity-related infertility assisted technologies enable more to become pregnant.
  • 14 - Glucocorticoids and placental programming
    pp 175-187
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    Summary

    This chapter considers the susceptibility of the early stages of mammalian development before embryo implantation, and even before fertilization has occurred. Maternal obesity and high body mass index (BMI) are associated with reduced fertility and an increased risk of miscarriage in both natural and assisted pregnancies. The pre-implantation embryo has received significant attention in recent years with respect to environmental effects on short- and long-term gestational development, and health into adulthood. Pre-implantation embryos during either early cleavage or until blastocyst formation are cultured in vitro for in vitro fertilization (IVF) and assisted reproductive technologies (ART) treatments. DNA methylation patterns are extensively remodeled during pre-implantation development, thereby providing a potential window for epigenetic sensitivity to environmental conditions. Maternal nutritional restriction during the periconceptional period leads to adverse developmental programming during fetal and postnatal life in domestic animal models.
  • 16 - The placental roots of cardiovascular disease
    pp 201-215
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    Summary

    This chapter reviews the key roles of the different layers of the maternofetal interface in supplying essential nutrients to the developing fetus before the placental circulations are fully established. Focal trophoblastic oxidative damage and progressive villous degeneration trigger the formation of the fetal membranes that remodel the uteroplacental interface. The distribution of the placental-specific protein human chorionic gonadotrophin (hCG) in yolk sac and coelomic fluid samples, and the absence of hCG mRNA expression in yolk sac tissue, suggests the secondary yolk sac (SYS) has an absorptive function. During the 10th week of gestation, the yolk sac starts to degenerate and rapidly ceases to function. The anatomy of the materno-fetal interface in the first trimester is the result of the need for a delicate balance between the metabolic requirements of the developing fetus and the potential harmful effects of oxygen during embryogenesis and organogenesis.
  • 18 - Final general discussion
    pp 229-232
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    Summary

    Imprinted genes are regulated by parent-of-origin-specific epigenetic marks, notably DNA methylation, leading to monoallelic expression of these genes in the offspring. All of these genes are conserved in mice and humans, although there are a few differences in imprinting status in the two species, with a slightly greater number of genes imprinted in mice than in humans. Given the frequent function as growth rheostats, imprinted genes are interesting candidates for a role in intrauterine growth restriction (IUGR). IUGR is a common medical condition that often leads to expensive neonatal hospitalization and predisposes to serious postnatal complications. Owing to their action in the placenta, there are a number of genetic models involving imprinted genes that already seem promising for investigating DOHAD. Very few genes are expressed only in the placenta, and even some legendary placenta specific genes are, in fact, expressed in the adult animal, an example being Ascl2.

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