Endovascular Trophoblast and PGE Synthesis

Endovascular Trophoblast and PGE synthesis

Endovascular trophoblast presumably derived from the cytotrophoblast shell appears within the
lumina of the decidual spiral arteries. This type of invasion seems to begin during the first month
of pregnancy. The relations of endovascular trophoblast with the spiral vessel walls shows
degenerative changes in the spiral vessel walls that is endothelial hypertrophy, muscular
retrogression and the appearance of swollen cells that are the consequence of the invasion of the
wall by the endovascular trophoblast cells (1).

A conspicuous feature of the human implantation site is the presence of trophoblast cells
(endovascular trophoblast) within the lumen of decidual spiral arteries. These trophoblast plugs are
continuous with the trophoblast shell occluding the orifice of the spiral arteries at the point of entry
to the inter villous space (Boyd and Hamilton) (2). The plugs consist of loosely cohesive cells
which move down the inner wall of the vessel like wax dripping down the side of a candle. These
loose plugs are thought to act as valves allowing plasma to seep into the inter villous space at low
pressures. In addition the trophoblast cells can be seen embedded in the walls of these spiral
arteries together with fibroid chains of musculo-elastic tissues to form spiral vessels into low
resistance sinusoid sacs which can maintain the utero-placental blood flow under all physiological
conditions (3).

Defective implantation

 

 

YOKE Y W, King A
Figure 1. Immunology of human placental implantation: clinical implications of our current understanding.
Molecular Medicine Today review 1997;3(4):153-159

Spiral arteries are functionally occluded by trophoblastic plugs. These are integral parts of the
trophoblastic shell. The cohesivity between trophoblastic cells within the plugs is rather loose.
Fluid and very small calibre particles can percolate through the plugs. The intra vascular
trophoblast plugs do not incorporate with the vessel wall, nor do they acquire tight junctions with
endothelial cells. This implies that they are loose and must act like valves. Direct observation with
the chorionscope confirms this fact. Spiral arteries run a very tortuous course which is subject to
continuous changes. Physiologically there are always necrotic foci within the decidua. Arterial
segments also undergo necrosis. There are however new channels which are open. In serial
reconstructions a given artery may be opened several times and occluded by several trophoblastic
plugs. The length of a spiral artery is the same at 8 weeks as it is at term (4).
In the first few months of pregnancy endovascular trophoblast is encountered in the decidual spiral
arteries but not beyond the decidual myometrial junction. At 16-18 weeks endovascular trophoblast
was noticed in the myometrial segments of many spiral arteries which means a second wave of
endovascular migration is triggered off quickly after a resting phase of several weeks (1).
Endovascular trophoblast cells stained positive of IL-!/FDG$6*(:>2'&4&-$@Q-1 stimulates PGE2 on
cell surfaces (6) .



REFERENCES

  1. PIJNENBORG R
    Trophoblast invasion and placentation in the human: morphological aspects
    Trophoblast research 1990;49:33-50.
  2. BOYD J D, HAMILTON W J 1970
    In the human placenta, Cambridge, W Heffer p365.
  3. BURROWS T D, KING A, LOKE Y W
    Expression of adhesion molecules by endovascular trophoblast and decidual endothelial cells: implications for vascular invasion during implantation.
    Placenta 1994;15:21-33.
  4. HUSTIN J
    The materno-trophoblastic interface: intro-placental blood flow, pages 97-110, in the first twelve weeks of gestation.
    Eds. Barnea E R, Hustin J, Jauniaux E, Springer-Verlag 1992.
  5. XAO-LING HU, YANG YA PING, HUNT J S
    Differential distribution of interleukin-1 alpha and interleukin-1 beta proteins in human placentas.
    J Reprod. Immunol. 1992;22:257-268.
  6. SIMON C, FRANCES A, PIQUETTE G, HENDRICKSON M, MILKI A, POLAN M L
    Interleukin-1 system in materno-trophoblast unit in human implantation. Immuno histochemical evidence for autocrine/paracrine function.
    J. Clin. Endocrinol. Metab. 1994;78:847-854

 

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