Figure 6
From: Impaired placental neovascularization in mice with pregnancy-associated hypertension
IUGR in PAH mice. (a) Significant numbers of nucleated RBCs are still detectable in PAH labyrinth at E19 (right). In some parts, nucleated RBCs are accumulated as an island (inset). (b) Mean number of nucleated RBCs in sagittal section, counted from ten specimens of each group is shown. (c) Comparison of sagittal body sections and the brains, lungs, kidneys and hearts between WT fetus (left) and PAH fetus (right) at E19. (d) Schema of pathological events in the placental labyrinth of PAH induced by RAS-mediated maternal hypertension. The downregulation of Ang/Tie system disrupts the interactions and crosstalk between ECs and pericytes. In addition, the downregulation of claudin-5, Apelin/APJ and eNOS on mid-pregnancy and the upregulation of ET-1 on later phase in PAH placenta enhance BP elevation and suppress the normal vascular maturation in placenta. These induce the poorly developed fetal vasculature, which cannot interact with maternal blood sinus appropriately, and lead to insufficient supply of oxygen and nutrients, resulting in the preeclamptic complications including maternal pathology and fetal IUGR.
