The Multiple Roles of EG-VEGF/PROK1 in Normal and Pathological Placental Angiogenesis
Figure 1
Proposed model of EG-VEGF-mediated effects on the fetomaternal angiogenesis during the first trimester of pregnancy. (a) and (b) represent cartoons of placental villi with EG-VEGF expression and actions on CT and EVT. (a) During the first trimester, EG-VEGF increases CT proliferation via PROKR1 activation and inhibits EVT invasion via PROKR2 activation. EG-VEGF/PROKR actions participate actively in trophoblastic shell and plugs constitution and contribute to the maintenance of physiological hypoxia during the first trimester of pregnancy. (b) At the end of the first trimester, EG-VEGF secretion declines. This contributes with other factors to EVT invasion and to the establishment of the fetomaternal circulation.
