The effect of dexamethasone on uterine receptivity, mediated by the ERK1/2-mTOR pathway, and the implantation window: An experimental study.

Background: The role of glucocorticoids in implantation has been demonstrated.

Objective: This study aimed to evaluate the effect of dexamethasone on endometrial receptivity.

Materials And Methods: In this experimental study, 40 BALB/c female mice aged eight wk old weighing approximately 25.

miR223-3p, HAND2, and LIF expression regulated by calcitonin in the ERK1/2-mTOR pathway during the implantation window in the endometrium of mice.

Problem: Approximately one-third of infertility cases are related to the female partner, and implantation failure is the primary reason for female infertility. The current research was established to assess the impact of calcitonin on endometrial receptivity.

Methods Of Study: 64 female BALB/c mice were assigned to 2 groups as follows: mice with regular ovarian cycle and mice with stimulated ovarian cycle.

Administration of dexamethasone disrupts endometrial receptivity by alteration of expression of miRNA 223, 200a, LIF, Muc1, SGK1, and ENaC via the ERK1/2-mTOR pathway.

Successful implantation of embryos requires endometrial receptivity. Glucocorticoids are one of the factors influencing the implantation window. In this study, 40 female BALB/c mice were used to study the impacts of dexamethasone administration on endometrial receptivity markers during implantation window.

The effect of fludrocortisone on the uterine receptivity partially mediated by ERK1/2-mTOR pathway.

Implantation of embryos needs endometrial receptivity. Mineralocorticoids is one of the causes influencing the implantation window. This study targeted to evaluation fludrocortisone different properties on endometrial receptivity.

Calcitonin administration improves endometrial receptivity via regulation of LIF, Muc-1 and microRNA Let-7a in mice.

Calcitonin (CT) is one of the factors affecting the embryo implantation, but its effects on the implantation window have not been fully investigated. The current study investigated the effects of CT on the endometrium receptivity by morphological study and evaluation of leukemia inhibitory factor (LIF), mucin 1 (Muc-1), and microRNA (miRNA) Let-7a in the ovarian stimulation and the normal ovarian cycle. Then the mechanism of the CT effects through the mammalian target of rapamycin (mTOR) signaling pathway was studied by using PP242.

Upregulation of HB-EGF, Msx.1, and miRNA Let-7a by administration of calcitonin through mTOR and ERK1/2 pathways during a window of implantation in mice.

Background: Successful implantation of embryos requires endometrial receptivity. Calcitonin is one of the factors influencing the implantation window. This study aimed to evaluate calcitonin effects on endometrial receptivity.

Semi-quantitative analysis of HOXA11, leukemia inhibitory factor and basic transcriptional element binding protein 1 mRNA expression in the mid-secretory endometrium of patients with endometriosis.

Background: HOXA11 and leukemia inhibitory factor (LIF) and basic transcriptional element binding protein1 (BTEB1) are expressed in endometrium throughout the menstrual cycle and show a dramatic increase during the mid-luteal phase at the time of implantation. In this case-control study, the expression pattern of these mRNA was evaluated in patients with endometriosis at the time of implantation. We also describe a semi-quantitative RT-PCR protocol optimized in our laboratory.