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Page 1 of 2

The Placenta and Human Developmental Programming
  • Edited by Graham J. Burton, David J. P. Barker, Ashley Moffett, Kent Thornburg
  • Published online: 04 February 2011
  • Print publication: 16 December 2010
  • 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.

  • 9 - The role of the maternal immune response in fetal programming

  • Edited by Graham J. Burton, David J. P. Barker, Ashley Moffett, Kent Thornburg
  • Book: The Placenta and Human Developmental Programming
  • Published online: 04 February 2011
  • Print publication: 16 December 2010, pp 102-113

  • 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.

  • 1 - Introduction

  • Edited by Graham J. Burton, David J. P. Barker, Ashley Moffett, Kent Thornburg
  • Book: The Placenta and Human Developmental Programming
  • Published online: 04 February 2011
  • Print publication: 16 December 2010, pp 1-4

  • 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.

  • 18 - Final general discussion

  • Edited by Graham J. Burton, David J. P. Barker, Ashley Moffett, Kent Thornburg
  • Book: The Placenta and Human Developmental Programming
  • Published online: 04 February 2011
  • Print publication: 16 December 2010, pp 229-232

  • 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.

  • Chapter 6 - Immune cells in the placental bed

  • from Section 3: - Uterine vascular environment
  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book: Placental Bed Disorders
  • Published online: 06 July 2010
  • Print publication: 03 June 2010, pp 41-51

  • Summary

    At the site where the placenta implants there is intermingling of fetal trophoblast cells with maternal tissues. Uterine natural killer (uNK) cells are defined by the high expression of the surface marker CD56 so they are designated CD56superbright. NK cells are not a feature of the myometrium so the behavior of trophoblast in the deeper part of the uterus is independent of their influence. A further potential site where maternal immune cells can interact with endovascular trophoblast is in the spiral arteries in the decidua basalis. All uNK cells express high levels of the inhibitory receptor CD94/NKG2A whose ligand is HLA-E. HLA-G is a non-classical HLA class I molecule that was identified and found to be expressed by trophoblast cells nearly 20 years ago. The overall conclusion is that the local immunity in the human implantation site is an unusual one that is reflected in the cell types present.

  • 6 - Immunological factors and placentation: implications for pre-eclampsia

  • from Part I - Basic science
  • Edited by Fiona Lyall, University of Glasgow, Michael Belfort, University of Utah
  • Book: Pre-eclampsia
  • Published online: 03 September 2009
  • Print publication: 10 May 2007, pp 92-102

  • Summary

    Introduction

    Pre-eclampsia only occurs during pregnancy, a physiological situation where allogeneic cells from two different individuals come into close contact. Furthermore, the development of the disease is dependent only on the presence of the placenta and not the fetus as the disease is frequently seen in complete hydatidiform mole where no fetus is present. Numerous epidemiological studies have given rise to the widely held view that immunological mechanisms probably contribute to the pathogenesis of this disease (and indeed other pregnancy disorders) (Dekker, 2002; Redman, 1991; Roberts and Lain, 2002; Walker, 2000). However, the molecular and biological mechanisms underlying this presumed maternal immune maladaptation remain unknown.

    During pregnancy both the maternal and fetal immune systems would be expected to recognize the presence of each other's allogeneic cells. However, the acceptance of the fetal allograft by the mother is at variance with the rejection typically seen with organ grafts. If the transplant analogy is extended further it would be expected that the maternal immune reaction would exhibit both specificity and memory for particular paternal genes expressed by the placenta. In other words, is there a partner-specific effect which contributes to pregnancy success or failure? Therefore, in considering possible immunological factors in pre-eclampsia two broad questions arise: first, how does the maternal immune system normally allow a symbiotic relationship with the feto-placental unit and, second, can this symbiosis be altered in a partner-specific way in pre-eclampsia?

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