Regulation of prostaglandin D synthase and prostacyclin synthase in the endometrium of cyclic, pregnant, and pseudopregnant rats and their regulation by sex steroids

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Abstract

Prostaglandins (PGs) are critical regulators of a number of reproductive processes. To date, the presence and regulation of PGS in the rat endometrium have not yet been described. The objective of the present study was to investigate the expression of PGD synthase (PGDS) and prostacyclin synthase (PGIS) in the endometrium. Endometrial proteins and tissues were collected from cyclic non-pregnant, pregnant, and steroid-induced pseuclopregnant rats. PGIS and PGDS were detected in the endometrium of cyclic, pregnant, and pseudopregnant rats but were not influenced by the estrous cycle. During early pregnancy, PGIS was significantly higher at day 5 and was gradually decreased from day 5.5 to 6.5. Later during pregnancy, PGIS was maximal on day 12 and gradually decreased to the end of pregnancy. PGDS expression was high during early and was maximal at the end of pregnancy. During pseudopregnancy, PGDS and PGIS were increased in a time-dependent manner and were maximal at day 5. Immunohistochemical analysis revealed that PGDS and PGIS were found in luminal as well as glandular epithelial cells and in stroma during late pregnancy. We also found a significant increase of PGD2 serum metabolite at days 21 and 22 of pregnancy. During steroid-induced pseudopregnancy, PGI2 serum metabolite was increased in a time-dependent manner and was maximal at day 7. These results suggest that PGDS and PGIS are present and could be regulated by steroids in the rat uterus during pregnancy, and that the endometrium could be a significant source of PGD2 and PGI2 at specific times during pregnancy. © 2007 Society for Endocrinology.

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Kengni, J. H. C., St.-Louis, I., Parent, S., Leblanc, V., Shooner, C., & Asselin, E. (2007). Regulation of prostaglandin D synthase and prostacyclin synthase in the endometrium of cyclic, pregnant, and pseudopregnant rats and their regulation by sex steroids. Journal of Endocrinology, 195(2), 301–311. https://doi.org/10.1677/JOE-07-0353

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