Our data show that PSG1 is involved in capillary morphogenesis and that it also influences vascular morphogenetic processes induced by VEGFA. PSG1 induced endothelial cell tube formation in the presence and absence of VEGFA. When VEGFA was added to the cells together with PSG1, we observed that the network was enhanced over the cells in which PSG1 or VEGFA was added alone. Further experiments are required to determine the molecular and signaling mechanisms by which PSG1 induces endothelial tube formation. Tube formation likely is not the result of induction of VEGFA by PSG1, because we did not observe significant PSG1-mediated VEGFA secretion in endothelial cells at PSG1 concentrations employed in the tube assays. Additionally, we did not observe an increase in endothelial cell migration upon PSG1 treatment, which would be expected as a result of up-regulation of VEGFA. Therefore, while PSG1 may increase the availability of VEGFA in the placenta, the effect on endothelial cells, because of its ability to induce VEGFA secretion from other cell types, may be of a paracrine nature or could be mediated by the observed up-regulation of TGFB1. PSGs belong to the CEA family, and it is interesting to note that other members of this family, which are membrane bound, have been implicated in the processes of immunoregulation, human trophoblast invasion, and angiogenesis [27, [56] [57] [58] [59] [60] [61] .