Using an autoantibody-induced animal model of preeclampsia, we show that AT(1)-AAs cross the mouse placenta, enter fetal circulation, and lead to small fetuses with organ growth retardation. AT(1)-AAs also induce apoptosis in the placentas of pregnant mice, human villous explants, and human trophoblast cells. Finally, autoantibody-induced IUGR and placental apoptosis are diminished by either losartan or an autoantibody-neutralizing peptide.
Hmmmm. This work's been going on for a few years now and this is a more explicit formulation of it than I've seen elsewhere. It looks like at least a partial explanation of IUGR may be this specific form of autoantibody that interferes with the normal blood pressure regulating mechanism -- and it crosses the placenta to do so -- as well as with the normal growth and development of the placenta.
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