Glycobiology World Congress

Biography

Biography: Regina Célia Teixeira Gomes

Abstract

Initially our group found out that the metoclopramide-induced hyperprolactinemia may negatively affect the endometrial morphology. And, in later studies we found out that the hyperprolactinemia caused a decrease in pinopode numbers and embryo implantation in female mice, thus interfering with the fertility and in ovarian function. In order to show the effectiveness of treatment with 200 µg metoclopramide for 50 consecutive days, we measured the serum prolactin levels and also analyzed the pituitary of animals. We proved that the hyperprolactinemia caused by metoclopramide in mice is due to an increase in the number and activity of lactotrophs. The deepening of the research led us to several questions. What are the biochemical changes that were occurring in the endometrial stroma (cells and extracellular matrix) of these animals? Finally, our results showed that the elevation of prolactin may lead to changes in the amounts of glycosaminoglycans, which are important for embryo implantation, in an animal model of hyperprolactinemia accompanied by a regular estrous cycle. Recently, we have researched the gene expression of small leucine-rich proteoglycans (SLRPs) on the murine uterus non pregnant and pregnant with hyperprolactinemia induced metoclopramide. The interactions between the production and degradation of these substances with steroids and hyperprolactinemia is complex and difficult to explain, because the signaling pathways involving those hormones may influence the cell-cell and cell-extracellular matrix interactions in the endometrial stroma, as well as they may interfere with the appropriate preparation of the endometrium to receive the embryo.