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Review
. 2000 Dec;157(6):1759-68.
doi: 10.1016/S0002-9440(10)64813-4.

Uteroplacental blood flow. The story of decidualization, menstruation, and trophoblast invasion

H J Kliman  1
Affiliations
Review

Uteroplacental blood flow. The story of decidualization, menstruation, and trophoblast invasion

H J Kliman. Am J Pathol. 2000 Dec.
No abstract available

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Figures

Figure 1.
Figure 1.
Pathways of trophoblast differentiation. Just as the undifferentiated basal layer of the skin gives rise to differentiated keratinocytes, the cytotrophoblast (the stem cell of the placenta) gives rise to the differentiated forms of trophoblasts. Left: Within the chorionic villi, cytotrophoblasts fuse to form the overlying syncytiotrophoblast. The villous syncytiotrophoblast makes the majority of the placental hormones, the most studied of which is human chorionic gonadotropin (hCG). Cyclic adenosine monophosphate (cAMP) and its analogues, and more recently hCG itself, have been shown to direct cytotrophoblast differentiation toward a hormonally active syncytiotrophoblast phenotype. Center: At the point where chorionic villi make contact with external extracellular matrix (decidual stromal ECM in the case of intrauterine pregnancies), a population of trophoblasts proliferates from the cytotrophoblast layer to form the second type of trophoblast, the junctional trophoblast. The junctional trophoblasts make a unique fibronectin, trophouteronectin (TUN), that appears to mediate the attachment of the placenta to the uterus. Transforming growth factor-β (TGFβ) and, more recently, leukemia inhibitory factor (LIF) have been shown to down-regulate hCG synthesis and up-regulate TUN secretion. Right: Finally, a third type of trophoblast, the invasive intermediate trophoblast, differentiates toward an invasive phenotype and leaves the placenta entirely. In addition to making human placental lactogen, these cells also make urokinase-type plasminogen activator and type 1 plasminogen activator inhibitor (PAI-1). Phorbol esters have been shown to increase trophoblast invasiveness in in vitro model systems and to up-regulate PAI-1 in cultured trophoblasts.
Figure 2.
Figure 2.
Invasive trophoblasts. Uterine spiral artery (V) containing maternal blood (M) from a 4-week pregnancy. The maternal endometrium (D) has become decidualized, meaning that the stromal cells have been transformed into large, pale cells (*). Infiltrating between these decidual cells are the invasive trophoblasts (some examples are highlighted by arrows) which have begun to modify the vessel wall (≈).
Figure 3.
Figure 3.
Failure of invasive trophoblasts to penetrate the maternal spiral arteries. Normally the invasive trophoblasts (T) infiltrate through the endo- and myometrium, reach the spiral arteries (*), and convert their muscular walls into pliant channels. In cases of preeclampsia, the trophoblasts often do not complete the final arterial penetration, possibly due to the maternal lymphocytes that commonly surround the spiral arteries. Compensatory maternal hypertension can lead to additional spiral artery damage or even occlusion. V, maternal uterine vein.
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References

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