Figure 7.

Proposed mechanisms driving localized decidualization in the cycling human endometrium. Prostaglandins can enhance the decidualization process in the human endometrium. In vivo, decidualization originates in the stroma surrounding the vascular endothelium. Activation of endothelial cells by physiological cues such as shear stress forces can induce the prostaglandin pathway in endothelial cells and promote the secretion of prostaglandins. Specifically, PGI₂ and to a certain extent PGE₂, but not PGD₂, can accelerate decidualization in adjacent endometrial stromal cells via their respective prostaglandin receptors. These events promote the enhanced response to progesterone (P4) via cAMP activation that lead to increased decidualization.