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5 results

  • Characterization of the role of microRNA-517a expression in low birth weight infants

  • G. Y. Song, W. W. Song, Y. Han, D. Wang, Q. Na
  • Journal:
    Journal of Developmental Origins of Health and Disease / Volume 4 / Issue 6 / December 2013
    Published online by Cambridge University Press:
    26 June 2013, pp. 522-526

  • The purpose of this study was to analyze the expression of the placenta-specific microRNA miR-517a in maternal serum and in placental tissue from low birth weight newborns and try to detect the effects of miR-517a expression on invasion potential of trophoblasts. Placental tissue and maternal serum were collected from both low birth weight newborns (n = 10) and normal birth weight newborns (n = 20). Expression of miR-517a was assessed in placenta and serum samples by real-time qRT-PCR. In addition, human trophoblast HTR8/SVneo cells were transfected with a miR-517a 2′-O-methyl oligonucleotide or a negative control RNA, and invasion was measured using transwell migration assays. Expression of miR-517a was significantly increased in placentas from low birth weight newborns (61.79 ± 23.06) in comparison with those of normal birth weight newborns (5.01 ± 1.97; P < 0.05). The expression of miR-517a was also increased in maternal serum isolated from the low birth weight newborn (25.78 ± 8.69) compared with the normal birth weight newborn (3.21 ± 1.07; P < 0.05). Overexpression of miR-517a significantly inhibited invasion of HTR8/SVneo cells (P < 0.05). These data indicate that miR-517a overexpression could potentially lead to low birth weight, likely through the inhibition of trophoblast invasion.

  • Chapter 16 - Fertile soil or no man’s land:

  • from Section 6: - Genetics
  • Edited by Robert Pijnenborg, Ivo Brosens, Roberto Romero
  • Book:
    Placental Bed Disorders
    Published online:
    06 July 2010
    Print publication:
    03 June 2010, pp 165-173

  • 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.

  • Chapter 8 - Oxygen delivery at the deciduoplacental interface

  • 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 63-74

  • Summary

    Placental vasculature, in particular the relationship between maternal and fetal blood circulations, has been a contentious issue for a long time. In his magnificent Anatomy of the human gravid uterus William Hunter included the first drawing of spiral arteries (convoluted arteries), in what must have been the very first illustration of a human placental bed. The French anatomist Mathias Duval was probably the first to recognize the invasion of trophoblast into endometrial arteries, in this case in the rat. It it became clear that deep trophoblast invasion and associated spiral artery remodeling are essential for a healthy pregnancy. The actual depth of invasion was underrated for a long time, partly because of the increasing popularity of the decidual barrier concept. Early observations of trophoblast invasion into the spiral arteries set the stage for understanding the maternal blood supply to the placenta via the spiral arteries of the placental bed.

  • 6 - Tissue remodelling the fetal-maternal interface: the regulation of matrix metalloproteinase 9 transcription

  • from SECTION 1 - PREPARATION FOR IMPLANTATION – THE UTERINE ENVIRONMENT
  • Edited by Hilary Critchley, University of Edinburgh, Iain Cameron, University of Southampton, Stephen Smith
  • Book:
    Implantation and Early Development
    Published online:
    05 June 2014
    Print publication:
    01 June 2005, pp 70-78

  • Summary

    This chapter deals with the regulation of matrix metalloproteinase-9 (MMP9) transcription in tissue remodelling at the fetal-maternal interface. MMPs, also called matrixins, are a family of at least 20 human zinc-dependent endopeptidases collectively capable of degrading all components of the endometrial extracellular matrix (ECM) essentially. Gelatinase B (MMP9) is considered to be instrumental in trophoblast invasion since in vitro, it mediates cytotrophoblastic cells (CTB) invasion into a Matrigel. The MMP9 gene contains 13 exons and 12 introns for a total size of 7.7 kbp. The regulatory region of this gene has been described in two studies showing multiple cis-regulatory elements. These cis-regulatory elements are specific DNA sequences that bind trans-activators or trans-repressors (transcription factors), which are thus proteins encoded by other genes. As is the case with many other genes, MMP9 can be regulated by co-repressors or coactivators.

  • 3 - Progestin-indusced decidualisation promotes human endometrial haemostasis and vascular stabulity

  • from SECTION 1 - PREPARATION FOR IMPLANTATION – THE UTERINE ENVIRONMENT
  • Edited by Hilary Critchley, University of Edinburgh, Iain Cameron, University of Southampton, Stephen Smith
  • Book:
    Implantation and Early Development
    Published online:
    05 June 2014
    Print publication:
    01 June 2005, pp 32-48

  • Summary

    This chapter focuses on the role of progestin-induced decidualisation in regulating endometrial haemostasis and vascular stability. Observations made by in situ hybridisation and immunohistochemistry of endometrial sections, together with in vitro studies of human endometrial stromal cells (HESCs), indicate that progest-ininduced decidualisation creates a pro-haemostatic, vascular-stabilising milieu that resists bleeding. During decidualisation of human endometrium, the interstitial-type extracellular matrix (ECM) of the follicular phase, which is enriched in fibronectin and collagen types I, III,V and VI, is converted to a mixture of residual interstitial proteins and new peridecidual basal laminar-type components. The resulting peridecidual cell ECM plays an integral role in implantation by modulating migration of the invading trophoblast and in counteracting the threat of local haemorrhage during endovascular trophoblast invasion by serving as a vascular support and stabilising scaffolding structure. Uterine natural killer (NK) cells have been implicated in maintaining decidualisation and in limiting trophoblast invasion.