Endometrial preparation: effect of estrogen dose and administration route on reproductive outcomes in oocyte donation cycles with fresh embryo transfer

Madero, Santiago; Rodríguez, Amelia; Vassena, Rita; Vernaeve, V.

doi:10.1093/humrep/dew099

Cited by 40 publications

(33 citation statements)

References 23 publications

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“…The present study provides insight into the mechanism by which down-regulation of decidual SGK1 by deregulated E 2 contributes to unexplained spontaneous miscarriage. E 2 supplementation has an impact on reproductive outcome, and benefits patients undergoing assisted reproductive technologies 59. As discussed in the present study, E 2 protects against pro-inflammatory immune responses at the feto-maternal interface, and represents a positive treatment for early threatened miscarriage.…”

Section: Discussionmentioning

confidence: 53%

Estradiol Suppresses TLR4-triggered Apoptosis of Decidual Stromal Cells and Drives an Anti-inflammatory T_H2 Shift by Activating SGK1

Lou¹,

Hu²,

Wang³

et al. 2017

Int. J. Biol. Sci.

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A pro-inflammatory cytokine profile at the feto-maternal interface may predispose immune maladaptation notably in early miscarriages. We investigated the involvement of estradiol (E2)-activated serum-glucocorticoid regulated kinase 1 (SGK1) in preserving the tolerogenic and pro-survival intrauterine microenvironment beneficial to gestation maintenance. Decidual SGK1 was down-regulated in early miscarriage, consistent with the lower serum E2 concentration seen in pregnancy loss. Lipopolysaccharide (LPS)/Toll-like receptors 4 (TLR4) signaling induced apoptosis and the pro-inflammatory T helper type (TH) 1 response of decidual stromal cells (DSCs) were associated with miscarriage. SGK1 activation was suppressed by LPS/TLR4 signaling and would be rescued by E2 administration via the PI3K signaling pathway in DSCs. SGK1 activation attenuated TLR4-mediated cell apoptosis, while promoting cell viability of DSCs by up-regulating the pro-survival genes BCL2 and XIAP, and enhancing the phosphorylation of FOXO1. Furthermore, E2-induced SGK1 activation reduced the secretion of pro-inflammatory TH1 cytokines, and promoted the generation of TH2 cytokines and elevated IRF4 mRNA and protein levels in LPS-incubated DSCs. Pharmacologic inhibition of SGK1 or suppression by small interfering (si) RNA increased the phosphorylation and nuclear translocation of NF-κB to reverse the pro-TH2 and anti-inflammatory effects of E2 pretreatment, leading to compromised pregnancy. These findings suggest that the E2-mediated SGK1 activation suppressed LPS-mediated apoptosis and promoted the anti-inflammatory TH2 responses in DSCs, ultimately contributing to a successful pregnancy.

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Section: Discussionmentioning

confidence: 53%

Estradiol Suppresses TLR4-triggered Apoptosis of Decidual Stromal Cells and Drives an Anti-inflammatory T_H2 Shift by Activating SGK1

Lou¹,

Hu²,

Wang³

et al. 2017

Int. J. Biol. Sci.

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“…To our knowledge, there is no study comparing oral and transdermal estrogen in non-donor FER cycles. However, in a recent large-scale retrospective case-control study encompassing 8362 fresh ET in donor cycles, no significant difference in live birth rate was found between oral (32.9 %) and transdermal (33.2 %) routes [65].…”

Section: Discussionmentioning

confidence: 91%

“…An additional preventive measure to further reduce the incidence of premature progesterone rise might be the use of higher estrogen starting doses (e.g., 6 mg daily from day 1 to day 3 of the cycle onwards), to further suppress gonadotropin release and prevent the occurrence of follicular dominance and excessive LH secretion [57]. However, in the above-mentioned large-scale retrospective case-control study encompassing 8362 fresh ET in donor cycles, employing AC with suppression, no significant difference in live birth rate was found between incremental or constant estrogen dosing [65].…”

Section: Discussionmentioning

confidence: 99%

Preparation of endometrium for frozen embryo replacement cycles: a systematic review and meta-analysis

Yaralı́

Polat

Mümüşoğlu

et al. 2016

J Assist Reprod Genet

109

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Purpose The purpose of this study was to evaluate the best protocol to prepare endometrium for frozen embryo replacement (FER) cycles. Methods This study is a systematic review and meta-analysis. Following PubMed and OvidSP search, a total of 1166 studies published after 1990 were identified following removal of duplicates. Following exclusion of studies not matching our inclusion criteria, a total of 33 studies were analyzed. Primary outcome measure was live birth. The following protocols, including true natural cycle (tNC), modified natural cycle (mNC), artificial cycle (AC) with or without suppression, and mild ovarian stimulation (OS) with gonadotropin (Gn) or aromatase inhibitor (AI), were compared. Results No statistically significant difference for both clinical pregnancy and live birth was noted between tNC and mNC groups. When tNC and AC without suppression groups are compared, there was a statistically significant difference in clinical pregnancy rate in favor of tNC, whereas it failed to reach statistical significance for live birth. When tNC and AC with suppression groups are compared, there was a statistically significant difference in live birth rate favoring the latter. Similar pregnancy outcome was noted among mNC versus AC with or without suppression groups. Similarly, no difference in clinical pregnancy and live birth was noted when ACs with or without suppression groups are compared. Conclusions There is no consistent superiority of any endometrial preparation for FER. However, mNC has several advantages (being patient-friendly; yielding at least equivalent or better pregnancy rates when compared with tNC and AC with or without suppression; may not require LPS). Mild OS with Gn or AI may be promising.

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“…The success of implantation relies on optimal cross-talk between embryo development and endometrial receptivity generally occurring between 6 and 10 days after ovulation. For endometrial preparation, the orchestrated control of estradiol (E2) and progesterone (P4) produced by the ovaries induces proliferative changes and development of a secretory phase, both required for 2 of 21 embryo-endometrial synchronicity [1]. Upon P4 stimulation, the process of decidualization begins with a complex and coordinated set of molecular events that result in endometrial receptivity [2].…”

Section: Well-functioning Endometrium Is Essential To Ensure Embryo Imentioning

confidence: 99%

Melatonin Promotes Uterine and Placental Health: Potential Molecular Mechanisms

Chuffa

Lupi

Cucielo

et al. 2019

IJMS

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The development of the endometrium is a cyclic event tightly regulated by hormones and growth factors to coordinate the menstrual cycle while promoting a suitable microenvironment for embryo implantation during the “receptivity window”. Many women experience uterine failures that hamper the success of conception, such as endometrium thickness, endometriosis, luteal phase defects, endometrial polyps, adenomyosis, viral infection, and even endometrial cancer; most of these disturbances involve changes in endocrine components or cell damage. The emerging evidence has proven that circadian rhythm deregulation followed by low circulating melatonin is associated with low implantation rates and difficulties to maintain pregnancy. Given that melatonin is a circadian-regulating hormone also involved in the maintenance of uterine homeostasis through regulation of numerous pathways associated with uterine receptivity and gestation, the success of female reproduction may be dependent on the levels and activity of uterine and placental melatonin. Based on the fact that irregular production of maternal and placental melatonin is related to recurrent spontaneous abortion and maternal/fetal disturbances, melatonin replacement may offer an excellent opportunity to restore normal physiological function of the affected tissues. By alleviating oxidative damage in the placenta, melatonin favors nutrient transfer and improves vascular dynamics at the uterine–placental interface. This review focuses on the main in vivo and in vitro functions of melatonin on uterine physiological processes, such as decidualization and implantation, and also on the feto-maternal tissues, and reviews how exogenous melatonin functions from a mechanistic standpoint to preserve the organ health. New insights on the potential signaling pathways whereby melatonin resists preeclampsia and endometriosis are further emphasized in this review.

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Endometrial preparation: effect of estrogen dose and administration route on reproductive outcomes in oocyte donation cycles with fresh embryo transfer

Abstract: None.

Cited by 40 publications

References 23 publications

Estradiol Suppresses TLR4-triggered Apoptosis of Decidual Stromal Cells and Drives an Anti-inflammatory T_H2 Shift by Activating SGK1

Estradiol Suppresses TLR4-triggered Apoptosis of Decidual Stromal Cells and Drives an Anti-inflammatory T_H2 Shift by Activating SGK1

Preparation of endometrium for frozen embryo replacement cycles: a systematic review and meta-analysis

Melatonin Promotes Uterine and Placental Health: Potential Molecular Mechanisms

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Endometrial preparation: effect of estrogen dose and administration route on reproductive outcomes in oocyte donation cycles with fresh embryo transfer

Abstract: None.

Cited by 40 publications

References 23 publications

Estradiol Suppresses TLR4-triggered Apoptosis of Decidual Stromal Cells and Drives an Anti-inflammatory TH2 Shift by Activating SGK1

Estradiol Suppresses TLR4-triggered Apoptosis of Decidual Stromal Cells and Drives an Anti-inflammatory TH2 Shift by Activating SGK1

Preparation of endometrium for frozen embryo replacement cycles: a systematic review and meta-analysis

Melatonin Promotes Uterine and Placental Health: Potential Molecular Mechanisms

Contact Info

Product

Resources

About

Estradiol Suppresses TLR4-triggered Apoptosis of Decidual Stromal Cells and Drives an Anti-inflammatory T_H2 Shift by Activating SGK1

Estradiol Suppresses TLR4-triggered Apoptosis of Decidual Stromal Cells and Drives an Anti-inflammatory T_H2 Shift by Activating SGK1