ABSTRACT
The placenta is a highly vascularized organ functioning as the interface between fetal
blood, which is confined within the villous blood vessels, and maternal blood, which
flows in decidual arteries and washes the intervillous spaces in contact with syncytiotrophoblast
(STB) cells. The STB adopts vascular characteristics such as the presence of von Willebrand
factor (vWF), CD31 markers, adhesion molecules, and coagulation components. The special
structure of the placenta requires efficient mechanisms for fast activation and localized
regulation of coagulation. The presence of procoagulant and anticoagulant components
on placental vascular endothelial cells (EC) and STB is essential for hemostasis.
Activation of coagulation may be a favored process, as suggested by elevated fibrin
depositions documented in some pathologic states. Increased localized procoagulant
components such as tissue factor (TF) and plasminogen activator inhibitors (PAI-1,
PAI-2), are associated with some pregnancy complications. Several anticoagulants regulate
placental coagulation: tissue factor pathway inhibitor (TFPI) is primarily produced
in EC; TFPI-2, a variant of TFPI, has been purified from the placenta and was identified
in the STB lining the villi; thrombomodulin, a membrane glycoprotein that activates
protein C, is localized in EC and apical membranes of STB; annexin V, an anticoagulant
that binds to negative membrane phospholipids, is abundant on normal placental STB,
whereas reduced STB annexin V was associated with the presence of antiphospholipid
antibodies. The placenta is a putative source of coagulation components. However,
the interplay between local procoagulant and anticoagulant mechanisms and their association
with pregnancy complications need to be assessed.
KEYWORDS
Placenta - procoagulants - anticoagulants - fibrinolysis - pregnancy complications