Prostaglandins and the initiation of blastocyst implantation and decidualization

Abstract

The process of blastocyst implantation in mammals is remarkably variable, especially in the extent of trophoblast invasion of the endometrium. In most species studied, the earliest macroscopically identifiable sign of blastocyst implantation is an increase in endometrial vascular permeability in areas adjacent to the blastocysts. This is followed in species with invasive implantation by decidualization, again localized to areas adjacent to the blastocysts. In some species, the application of a stimulus to the endometrium can result in increased endometrial vascular permeability and decidualization. Based initially on studies utilizing inhibitors of prostaglandin (PG) synthesis and more recently on studies using the techniques of transgenics, considerable evidence has accumulated indicating that PGs have an important role in the early events of implantation and artificially induced decidualization. However, which PGs are involved remains controversial. There may be differences between species, and different PGs may be involved at different times.

Hmgn1 acts downstream of C/EBPβ to regulate the decidualization of uterine stromal cells in mice

“…6 In the uterine stromal cells treated with estrogen plus progesterone, Hmgn1 could stimulate the expression of Cox-2 which was a rate-limiting enzyme in the biosynthesis of prostaglandins (PGs) and implicated in mouse decidualization. 25,26 Targeted disruption of Cox-2 led to defective decidualization. 25 Under artificially induced decidualization, Cox-2 inhibitor nimesulide diminished the production of uterine PGE 2 which was important for decidualization.…”

“…25 Under artificially induced decidualization, Cox-2 inhibitor nimesulide diminished the production of uterine PGE 2 which was important for decidualization. 26,27 mPGES-1 might catalyze the conversion of PGH 2 to PGE 2 and was also modulated by Hmgn1 during in vitro decidualization. 26 Cumulative evidences have declared that deficiency of Cox-2 or mPGES-1 caused a reduction in uterine Vegf mRNA level.…”

“…26,27 mPGES-1 might catalyze the conversion of PGH 2 to PGE 2 and was also modulated by Hmgn1 during in vitro decidualization. 26 Cumulative evidences have declared that deficiency of Cox-2 or mPGES-1 caused a reduction in uterine Vegf mRNA level. 28,29 Vegf was a well-known angiogenesis promoter and could profoundly influence the uterine angiogenesis which was crucial to decidualization.…”

Expression patterns and role of prostaglandin-endoperoxide synthases, prostaglandin E synthases, prostacyclin synthase, prostacyclin receptor, peroxisome proliferator-activated receptor delta and retinoid x receptor alpha in rat endometrium during artificially-induced decidualization

“…In rodents, this step is followed by proliferation and differentiation of endometrial stromal cells into decidual cells, a process termed decidualization (reviewed by Kennedy et al 2007). In addition, the endometrium of rodents responds to non-specific stimuli with increased EVP and subsequent decidualization provided that the stimulus is applied at the appropriate time (Psychoyos 1973).…”

“…Previous studies conducted in various species have shown that during pregnancy, the levels of prostaglandins (PGs) are elevated at implantation sites, suggesting a role of PGs in implantation (reviewed by Kennedy et al 2007). Moreover, numerous studies have shown that administration of inhibitors of PG synthesis and PG antagonists can inhibit or delay the initiation of implantation (reviewed by Kennedy et al 2007).…”