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

Niknafs B, Naser Shokrzadeh, Reza Alivand M, Bakhtiar Hesam Shariati M
International journal of reproductive biomedicine · 2022 · doi:10.18502/ijrm.v20i1.10408 · PMID:35308329 · PMC8902795
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This experimental study found that dexamethasone diminishes uterine receptivity in mice by downregulating key genes and miRNAs, an effect mediated through the ERK1/2-mTOR pathway.

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This experimental study investigated the impact of dexamethasone on uterine receptivity and implantation windows in pregnant BALB/c mice by analyzing molecular changes in the ERK1/2-mTOR signaling pathway. The researchers administered dexamethasone with or without the mTOR inhibitor PP242, then measured gene expression levels of HB-EGF, Msx-1, HAND2, and specific microRNAs alongside protein phosphorylation in endometrial tissue. Results indicated that dexamethasone significantly altered the expression of key implantation-related genes and reduced mTOR phosphorylation, effects that were partially reversed when the mTOR pathway was inhibited. Relevance to endometriosis: miRNA-451 is mentioned as essential for the growth and survival of endometriosis implants, linking this mechanistic study of uterine receptivity to the pathophysiology of endometriosis.

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Abstract

BackgroundThe role of glucocorticoids in implantation has been demonstrated.ObjectiveThis study aimed to evaluate the effect of dexamethasone on endometrial receptivity.Materials and methodsIn this experimental study, 40 BALB/c female mice aged eight wk old weighing approximately 25.0 ± 1.4 gr were used. The mice were divided into four groups (n = 10/each) of control, dexamethasone (100 μg/kg, intraperitoneal injection), mammalian target of rapamycin (mTOR) inhibitor (PP242) (30 mg/kg, intraperitoneal injection), and dexamethasone and PP242. The endometrial epithelium of the mouse was separated to measure messenger RNA expression of heart and neural crest derivatives-expressed protein 2 (HAND2), Msh homeobox 1 (Msx-1), heparin binding epidermal growth factor (HB-EGF), microRNA (miRNA) Let-7a, miRNA-145 and miRNA-451, using real-time polymerase chain reaction. Also, protein expression of mammalian mTOR and eukaryotic translation initiation factor 4E-binding protein1 (4E-BP1) was measured using western blot.ResultsThe results revealed that the expression of Msx-1, HAND2, HB-EGF, miRNA-451, and miRNA-Let-7a was significantly decreased in the endometrium in the dexamethasone group compared to the control, while the expression of miRNA-145 in the endometrium was up-regulated. Additionally, the administration of PP242, known as an inhibitor of mTOR, was associated with significantly reduced expression of Msx-1, HAND2, HB-EGF, miRNA-451, and miRNA-Let-7a, while PP242 induced messenger RNA expression of miRNA-145.ConclusionIt appears that dexamethasone can diminish uterine receptivity during the implantation period, at least to some extent, through the alteration of particular genes that impact endometrial receptivity. Furthermore, the mTOR pathway seemingly showed an essential role in endometrial receptivity.
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Our research has shown that dexamethasone reduces the expression of genes that impact mice uterine receptivity during implantation. It seems that such a decline in the expression of the above genes might be interceded by the mTOR signaling pathway, which could result in altered endometrial receptivity in normal cycles.

Coi Statement

The authors declare that there is no conflict of interest that prejudices the impartiality of this scientific work.

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