Abstract
BackgroundTo study the expression of Plexin-B1, Glycodelin, and MMP7 during the menstrual cycle in the endometrium and in the fallopian tube.MethodsThe research included women undergoing hysterectomy, tubal sterilization or salpingo-oophoerectomy. Total RNA from endometrial and fallopian tube tissues was extracted using a total RNA isolation kit. Semi-quantitative RT-PCR was performed to examine mRNA relative expression.ResultsPlexin-B1 expression in the endometrium was significantly higher on days 19 - 23 compared to days 12 - 14 (1.166 +/- 0.42 versus 0.523 +/- 0.299), P < 0.005. In the fallopian tube the level of plexin-B1 did not change significantly throughout the menstrual cycle. Glycodelin expression was significantly higher on days 19 - 23 compared with days 12-14, both in the endometrium (0.819 +/- 0.564 versus 0.072 +/- 0.343, P < 0.05) and the fallopian tube (0.796 +/- 0.196 versus 0.329 +/- 0.398, P < 0.05). Although the level of MMP7 secretion was the highest in the secretory phase the difference from the proliferative phase did not reach statistical significance, neither in the endometrium nor in the fallopian tube. This could result from a lack of power.ConclusionsIn the endometrium, both Glycodelin and Plexin-B1 are exhibiting a cyclic pattern suggesting a possible steroid regulation and a role in endometrial receptivity.
Highlights
To study the expression of Plexin-B1, Glycodelin, and Matrix metalloproteinase 7 (MMP7) during the menstrual cycle in the endometrium and in the fallopian tube
We investigated the expression in the endometrium and the fallopian tube of three genes, proposed to be involved in endometrial receptivity and maternal-trophoblastic interactions
Glycodelin expression during the menstrual cycle in the human endometrium and fallopian tube A total of 22 endometrial and fallopian tube biopsies were analyzed for Glycodelin expression
Summary
To study the expression of Plexin-B1, Glycodelin, and MMP7 during the menstrual cycle in the endometrium and in the fallopian tube. Implantation in humans involves complex interactions between the embryo and the maternal endometrium. The molecular mechanisms by which the surface of the human endometrium acquires morphological changes, leading to receptive features, are still unclear. Growth factors, hormones, extracellular matrix proteins and enzymes, angiogenic factors, cell-cell adhesion molecules and receptors are all involved in this complex process [1,2,3,4,5]. The endometrium is receptive to embryonic implantation during a defined window that is temporally and spatially restricted [1,2,3,4,5]. Coordinated effects of ovarian progesterone and estrogen play critical roles in establishing uterine receptivity for implantation [1,2,3,4,5]
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