Deportation of trophoblast and preeclampsia

Abstract

The trophoblasts play a key role in the pathogenesis of preeclampsia, especially the villous trophoblast. Its deportation in the maternal circulation is discussed in connection with the fusion of
cytotrophoblast with the syncytiotrophoblast as
well as apoptosis, necrosis or aponecrosis of the
syncytiotrophoblast. These mechanisms are altered
in preclinical and clinical phases of the disease. The alternating phases of hypoxia and re-oxygenation in the intervillous space, accelerated the
deportation of syncytiotrophoblast which affects
the maternal vascular endothelium and partly
explains the hypertension and its consequences.
Excess of syncytiotrophoblast debris observed in
maternal plasma or perfused human placenta were
involved. Their isolation has helped to highlight
multi-nucleated or mononucleated cells, microparticles and nanoparticles. The cells are eliminated
by the lungs, the microparticles are pro-inflammatory, pro-coagulant and anti-angiogenic. The
nanoparticles, formed mainly of exosomes constitute a new system of intercellular communication
actively explored because of its role in many
processes: viral infection, cancer and neurodegeneration. Their involvement in angiogenesis,
steroidogenesis or mother-fetus tolerance suggests
they may play a role in preeclampsia.