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Review
. 2011 Jul 16;11(1):27-36.
doi: 10.1007/s12522-011-0102-9. eCollection 2012 Jan.

Mechanism of maternal vascular remodeling during human pregnancy

Yukiyasu Sato  1 , Hiroshi Fujiwara  1 , Ikuo Konishi  1
Affiliations
Review

Mechanism of maternal vascular remodeling during human pregnancy

Yukiyasu Sato et al. Reprod Med Biol. .

Abstract

Remodeling of maternal spiral arteries by invasion of extravillous trophoblast (EVT) is crucial for an adequate blood supply to the fetus. EVT cells that migrate through the decidual tissue destroy the arterial muscular lining from the outside (interstitial invasion), and those that migrate along the arterial lumen displace the endothelium from the inside (endovascular invasion). Numerous factors including cytokines/growth factors, chemokines, cell adhesion molecules, extracellular matrix-degrading enzymes, and environmental oxygen have been proposed to stimulate or inhibit the differentiation/invasion of EVT. Nevertheless, it is still difficult to depict overall pictures of the mechanism controlling perivascular and endovascular invasion. Potential factors that direct interstitial trophoblast towards maternal spiral artery are relatively high oxygen tension in the spiral artery, maternal platelets, vascular smooth muscle cells, and Eph/ephrin system. On the other hand, very little is understood about endovascular invasion except for the involvement of endothelial apoptosis in this process. Only small numbers of molecules such as polysialylated neural cell adhesion molecules and CCR1 have been suggested as specific markers for the endovascular trophoblast. Therefore, an initial step to approach the mechanisms for endovascular invasion could be more detailed molecular characterization of the endovascular trophoblast.

Keywords: Endovascular trophoblast; Extravillous trophoblast; Interstitial trophoblast; Oxygen; Platelet.

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Figures

Figure 1
Figure 1
Schematic representation of early human placenta. In floating villus, cytotrophoblast (CTB) differentiates into multinucleated syncytiotrophoblast, where exchange of gas and nutrients takes place. At villus‐anchoring sites, CTB differentiates into extravillous trophoblast and forms the stratified structure called cell column. Extravillous trophoblast acquires invasive activity in the cell column. Neighboring cell columns fuse with one another to create the trophoblastic shell that covers the surface of maternal tissue. From the end of the cell column and trophoblastic shell, extravillous trophoblast begins to migrate through the decidual tissue (interstitial trophoblast) or along the lumen of spiral arteries in a retrograde manner (endovascular trophoblast)
Figure 2
Figure 2
Proposed events during maternal spiral artery remodeling. a Unremodeled artery. Decidual leukocytes (DLs) mainly composed of uterine natural killer cells and macrophages can be observed in the vicinity of the spiral artery. b Decidua‐associated (trophoblast‐independent) remodeling. Infiltration of DLs into arterial wall causes disruption and partial loss of vascular smooth muscle cell (VSMC) layer along with endothelial cell (EC) swelling. This remodeling process occurs prior to the arrival of extravillous trophoblast. c Trophoblast‐dependent remodeling. Interstitial trophoblast destroys VSMC layer from outside the artery and endovascular trophoblast replaces ECs from the inside. Endovascular invasion only occurs in the arteries surrounded and remodeled by the interstitial trophoblast. Note that DL is absent from the arterial wall at this stage
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References

    1. Pijnenborg R, Dixon G, Robertson WB, Brosens I. Trophoblastic invasion of human decidua from 8 to 18 weeks of pregnancy. Placenta, 1980, 1 (1) 3–19 10.1016/S0143‐4004(80)80012‐9 - DOI - PubMed
    1. Shih JC, Chien CL, Ho HN, Lee WC, Hsieh FJ. Stellate transformation of invasive trophoblast: a distinct phenotype of trophoblast that is involved in decidual vascular remodelling and controlled invasion during pregnancy. Hum Reprod, 2006, 21 (5) 1299–1304 10.1093/humrep/dei489 - DOI - PubMed
    1. Enders AC, Lantz KC, Schlafke S. Preference of invasive cytotrophoblast for maternal vessels in early implantation in the macaque. Acta Anat (Basel), 1996, 155 (3) 145–162 10.1159/000147800 - DOI - PubMed
    1. Burton GJ, Jauniaux E, Watson AL. Maternal arterial connections to the placental intervillous space during the first trimester of human pregnancy: the Boyd collection revisited. Am J Obstet Gynecol, 1999, 181 (3) 718–724 10.1016/S0002‐9378(99)70518‐1 - DOI - PubMed
    1. Coppens M, Loquet P, Kollen M, Neubourg F, Buytaert P. Longitudinal evaluation of uteroplacental and umbilical blood flow changes in normal early pregnancy. Ultrasound Obstet Gynecol, 1996, 7 (2) 114–121 10.1046/j.1469‐0705.1996.07020114.x - DOI - PubMed