[Defective placental implantation and its effects on maternal endothelial function]

Jean-Michel Foidart, Agnès Noël, Frédéric Chantraine, Sophie Lorquet, Philippe Petit, Carine Munaut, Sarah Berndt, Christel Pequeux, Jean-Pierre Schaaps
Bulletin de L'Académie Nationale de Médecine 2009, 193 (5): 1059-64; discussion 1064-6, 1067-8
Preeclampsia, a pregnancy-specific syndrome characterized by hypertension, edema and proteinuria, resolves spontaneously on placental delivery. Its pathogenesis is thought to involve placental hypoxia, which leads to maternal vascular dysfunction through increased placental release of anti-angiogenic factors such as the soluble form of VEGF receptor-1 (VEGFR1). VEGFR1 binds VEGF and PIGF, which are also produced by villous trophoblastic cells. In the absence of VEGF and PIGF in the maternal circulation, endothelial dysfunction occurs in several vascular territories (liver, kidneys, brain, heart, lungs, etc.). In experimental models, sVEGFR1 not only has an anti-angiogenic action but also augments endothelial expression of NO synthase through intracellular transduction. When NO production is increased, pericytes and perivascular smooth muscle cells are recruited and their adhesion to endothelial cells is strongly stimulated. This can hinder both trophoblast invasion and increase uteroplacental flow during preeclampsia.

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