Uterine angiogenesis during implantation and decidualization in mice.

Abstract

Increased uterine vascular permeability and angiogenesis are hallmarks of implantation and placentation. These events are profoundly influenced by vascular endothelial growth factor (VEGF). Although VEGF and its receptor Flk-1 are primarily important for uterine vascular permeability and angiogenesis before and during the attachment phase of the implantation process, VEGF together with the angiopoietins and their receptor Tie-2 directs angiogenesis during decidualization after implantation. Uterine expression of HIF and ARNT follows the localization of VEGF expression with increasing angiogenesis during the postimplantation period, although their expression does not correlate with VEGF expression during the pre-implantation period. Upstream of VEGF, estrogen promotes uterine vascular permeability but inhibits angiogenesis, whereas progesterone stimulates angiogenesis with little effect on vascular permeability. Furthermore, COX-2-derived prostaglandins participate in uterine vascular permeability and angiogenesis during implantation and decidualization. (Reprod Med Biol 2006; 5: 81-86).