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
