Role of PTGS2 and PTGES in Receptivity and Initiation of Decidualization in Rat Endometrium.

Implantation is a complex process involving many physiological events including uterine receptivity follow by blastocyst attachment, apoptosis of endometrial luminal epithelium, an increase in endometrial vascular permeability, and finally decidualization. Previous studies conducted in this laboratory suggest that prostaglandin E2 (PGE2) but not prostaglandin I2 (PGI2) has a major role in the early events of implantation in the rat endometrium (Gillio-Meina et al 2007, 53rd Annual Meeting of the Canadian Fertility and Andrology Society, poster FP21). To further elucidate if PGE2 is involved in uterine receptivity and initiation of decidualization, we determined the temporal and spatial pattern of endometrial expression of genes encoding enzymes involved in PGE2 synthesis (prostaglandin-endoperoxide synthase 1 and 2 [PTGS1 and PTGS2], and microsomal and cytosolic prostaglandin E synthases [PTGES, PTGES2 and PTGES3]) in ovariectomized rats treated on the afternoon of the equivalent of day 4 of pseudopregnancy with estradiol (E2) and progesterone (P4), equivalent to nidatory E2 to induce receptivity), or P4 alone (to maintain the neutral state). Endometrium was separated from myometrium at 0, 5 or 15 h after the hormone injections and RNA and protein were isolated. Western blot analysis showed a significant increase in PTGES2 protein levels at 5 h in the presence of both E2 and P4, and at 15 h in the presence of P4 alone or in combination with E2. Moreover, PTGS2 protein levels were significantly higher 15 h after the treatment with both E2 and P4. To further study the role of PGE2 during initiation of decidualization, ovariectomized rats were treated with E2 and P4 to mimic pseudopregnancy and on day 5 of pseudopregnancy a bilateral intrauterine injection of sesame oil was given as a deciduogenic stimulus. Endometrial RNA and protein were isolated and uterine sections were prepared at 0 and at 2, 4, 8, 16 or 32 h following the stimulus. We found that Ptgs2 mRNA also significantly increased at 2 and 4 h after the deciduogenic stimulus, whereas the protein was upregulated at 8, 16 and 32 h. In addition, PTGES2 protein was upregulated at 2 and 4 h, whereas PTGES3 protein was significantly higher at 2, 4 and 8 h. By immunohistochemistry, PTGS1, PTGES2 and PTGES3 were co-localized in glands and luminal epithelium at all times, but the signals appeared to be higher at 2 and 4 h after the stimulus. By contrast, PTGS2 was localized in the stromal cells and the signal increased at 16 and 32 h. Because PTGS2 protein levels are increased by nidatory E2, it is possible that a product of that increase, PGE2, could be necessary for initiation of decidualization. Moreover, the upregulation of PTGES2 and PTGES3 proteins in the early stages of decidualization and an upregulation of PTGS2 in the later stages of decidualization, provides additional evidence that PGE2 is the PG most likely involved in decidualization in rat endometrium. [This work was supported by the Canadian Institutes of Health Research.]

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