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CC BY-NC-ND 4.0 · AJP Rep 2018; 08(04): e241-e246
DOI: 10.1055/s-0038-1675348
Case Report
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Decidual Vasculopathy in Preeclampsia and Spiral Artery Remodeling Revisited: Shallow Invasion versus Failure of Involution

Peilin Zhang
1   Department of Pathology, NYP Brooklyn Methodist Hospital, Brooklyn, New York
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Publikationsverlauf

27. Juni 2018

10. September 2018

Publikationsdatum:
18. Oktober 2018 (online)

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Abstract

Decidual vasculopathy is commonly associated with preeclampsia and develops in the late pregnancy in the uterine spiral arteries, which were previously remodeled by the extravillous trophoblasts. In normal early pregnancy, trophoblasts invade into the spiral artery, leading to vascular transformation, and this transformation is found to be associated with phenotypic switch of the endovascular trophoblasts to express CD56, a maternal protein likely from the natural killer (NK) cells. These endovascular trophoblasts are diminished at term. The decidual vessels are also returned to near normal at the delivery. Both the uterus and the uterine spiral arteries undergo involution after delivery. In preeclampsia, the endovascular trophoblasts are present within the vessel wall associated with the persistence of switched phenotype similar to those seen in the early implantation. The persistence of the endovascular trophoblasts in decidual vasculopathy indicates a failure to return to normal vessels in preeclampsia, thus suggesting a potential mechanism of pathogenesis. NK cells seem critical not only for early implantation and spiral artery remodeling but also for the development of decidual vasculopathy in preeclampsia. In this short review, some critical aspects of decidual vasculopathy in normal pregnancy and preeclampsia are reexamined and a new hypothesis is proposed.

Keywords

decidual vasculopathy - preeclampsia - CD56 - natural killer - spiral artery remodeling - involution
 

  • References

  • 1 Lisonkova S, Joseph KS. Incidence of preeclampsia: risk factors and outcomes associated with early- versus late-onset disease. Am J Obstet Gynecol 2013; 209 (06) 544.e1-544.e12
    CrossrefPubMedSuche in Google Scholar
  • 2 Mustafa R, Ahmed S, Gupta A, Venuto RC. A comprehensive review of hypertension in pregnancy. J Pregnancy 2012; 2012: 105918
    PubMedSuche in Google Scholar
  • 3 Valensise H, Vasapollo B, Gagliardi G, Novelli GP. Early and late preeclampsia: two different maternal hemodynamic states in the latent phase of the disease. Hypertension 2008; 52 (05) 873-880
    CrossrefPubMedSuche in Google Scholar
  • 4 Crispi F, Domínguez C, Llurba E, Martín-Gallán P, Cabero L, Gratacós E. Placental angiogenic growth factors and uterine artery Doppler findings for characterization of different subsets in preeclampsia and in isolated intrauterine growth restriction. Am J Obstet Gynecol 2006; 195 (01) 201-207
    CrossrefPubMedSuche in Google Scholar
  • 5 Benirschke K, Burton GJ, Baergen RN. eds. Pathology of the Human Placenta. Berlin: Springer Verlag; 2012
    PubMedSuche in Google Scholar
  • 6 Zhang P, Schmidt M, Cook L. Maternal vasculopathy and histologic diagnosis of preeclampsia: poor correlation of histologic changes and clinical manifestation. Am J Obstet Gynecol 2006; 194 (04) 1050-1056
    CrossrefPubMedSuche in Google Scholar
  • 7 Hertig A. Vascular pathology in the hypertensive albuminuric toxemias of pregnancy. Clinics 1945; 4: 602-614
    PubMedSuche in Google Scholar
  • 8 Marais W. Human decidual spiral artery studies–part i. Int J Obstet Gynecol 1962; 69 (02) 1-12
    PubMedSuche in Google Scholar
  • 9 Marais W. Human decidual spiral arterial studies–part ii. Int J Obstet Gynecol 1962; 69 (02) 213-224
    PubMedSuche in Google Scholar
  • 10 Staff AC, Dechend R, Pijnenborg R. Learning from the placenta: acute atherosis and vascular remodeling in preeclampsia-novel aspects for atherosclerosis and future cardiovascular health. Hypertension 2010; 56 (06) 1026-1034
    CrossrefPubMedSuche in Google Scholar
  • 11 Robertson WB, Brosens I, Dixon HG. The pathological response of the vessels of the placental bed to hypertensive pregnancy. J Pathol Bacteriol 1967; 93 (02) 581-592
    CrossrefPubMedSuche in Google Scholar
  • 12 Pijnenborg R, Vercruysse L, Hanssens M, Brosens I. Endovascular trophoblast and preeclampsia: a reassessment. Pregnancy Hypertens 2011; 1 (01) 66-71
    CrossrefPubMedSuche in Google Scholar
  • 13 Brosens I, Robertson WB, Dixon HG. The physiological response of the vessels of the placental bed to normal pregnancy. J Pathol Bacteriol 1967; 93 (02) 569-579
    CrossrefPubMedSuche in Google Scholar
  • 14 Kam EP, Gardner L, Loke YW, King A. The role of trophoblast in the physiological change in decidual spiral arteries. Hum Reprod 1999; 14 (08) 2131-2138
    CrossrefPubMedSuche in Google Scholar
  • 15 Zhang P. . CD56 expression of intravascular trophoblasts defines a class of vasculopathy in preeclampsia and other pregnancy complications. https://www.biorxiv.org/content/biorxiv/early/2018/04/01/293027.full.pdf 2018 . Accessed October 16, 2018
    PubMed
  • 16 Waite LL, Atwood AK, Taylor RN. Preeclampsia, an implantation disorder. Rev Endocr Metab Disord 2002; 3 (02) 151-158
    CrossrefPubMedSuche in Google Scholar
  • 17 Khong TY, Mooney EE, Ariel I. , et al. Sampling and definitions of placental lesions: Amsterdam placental workshop group consensus statement. Arch Pathol Lab Med 2016; 140 (07) 698-713
    CrossrefPubMedSuche in Google Scholar
  • 18 Hecht JL, Zsengeller ZK, Spiel M, Karumanchi SA, Rosen S. Revisiting decidual vasculopathy. Placenta 2016; 42: 37-43
    PubMedSuche in Google Scholar
  • 19 Croy BA, Ashkar AA, Minhas K, Greenwood JD. Can murine uterine natural killer cells give insights into the pathogenesis of preeclampsia?. J Soc Gynecol Investig 2000; 7 (01) 12-20
    CrossrefPubMedSuche in Google Scholar
  • 20 Ashkar AA, Di Santo JP, Croy BA. Interferon gamma contributes to initiation of uterine vascular modification, decidual integrity, and uterine natural killer cell maturation during normal murine pregnancy. J Exp Med 2000; 192 (02) 259-270
    CrossrefPubMedSuche in Google Scholar
  • 21 Redline RW, Boyd T, Campbell V. , et al; Society for Pediatric Pathology, Perinatal Section, Maternal Vascular Perfusion Nosology Committee. Maternal vascular underperfusion: nosology and reproducibility of placental reaction patterns. Pediatr Dev Pathol 2004; 7 (03) 237-249
    CrossrefPubMedSuche in Google Scholar
  • 22 Norwitz ER, Schust DJ, Fisher SJ. Implantation and the survival of early pregnancy. N Engl J Med 2001; 345 (19) 1400-1408
    CrossrefPubMedSuche in Google Scholar
  • 23 Chakraborty D, Rumi MA, Konno T, Soares MJ. Natural killer cells direct hemochorial placentation by regulating hypoxia-inducible factor dependent trophoblast lineage decisions. Proc Natl Acad Sci U S A 2011; 108 (39) 16295-16300
    CrossrefPubMedSuche in Google Scholar
  • 24 Golic M, Haase N, Herse F. , et al. Natural killer cell reduction and uteroplacental vasculopathy. Hypertension 2016; 68 (04) 964-973
    CrossrefPubMedSuche in Google Scholar
  • 25 Colucci F. The role of KIR and HLA interactions in pregnancy complications. Immunogenetics 2017; 69 (8-9): 557-565
    CrossrefPubMedSuche in Google Scholar
  • 26 Moffett A, Colucci F. Uterine NK cells: active regulators at the maternal-fetal interface. J Clin Invest 2014; 124 (05) 1872-1879
    CrossrefPubMedSuche in Google Scholar
  • 27 Béziat V, Hilton HG, Norman PJ, Traherne JA. Deciphering the killer-cell immunoglobulin-like receptor system at super-resolution for natural killer and T-cell biology. Immunology 2017; 150 (03) 248-264
    PubMedSuche in Google Scholar
  • 28 Moffett A, Chazara O, Colucci F. Maternal allo-recognition of the fetus. Fertil Steril 2017; 107 (06) 1269-1272
    CrossrefPubMedSuche in Google Scholar
  • 29 Hiby SE, Walker JJ, O'shaughnessy KM. , et al. Combinations of maternal KIR and fetal HLA-C genes influence the risk of preeclampsia and reproductive success. J Exp Med 2004; 200 (08) 957-965
    CrossrefPubMedSuche in Google Scholar
  • 30 Hiby SE, Apps R, Sharkey AM. , et al. Maternal activating KIRs protect against human reproductive failure mediated by fetal HLA-C2. J Clin Invest 2010; 120 (11) 4102-4110
    CrossrefPubMedSuche in Google Scholar
  • 31 Hiby SE, Regan L, Lo W, Farrell L, Carrington M, Moffett A. Association of maternal killer-cell immunoglobulin-like receptors and parental HLA-C genotypes with recurrent miscarriage. Hum Reprod 2008; 23 (04) 972-976
    CrossrefPubMedSuche in Google Scholar
  • 32 Colucci F, Traherne J. Killer-cell immunoglobulin-like receptors on the cusp of modern immunogenetics. Immunology 2017; 152 (04) 556-561
    PubMedSuche in Google Scholar