ArticleReproductive biology and endocrinology : RB&E2022
GnRH antagonist weakens endometrial stromal cells growth ability by decreasing c-kit receptor expression.
Article in Reproductive biology and endocrinology : RB&E, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- The association of endometrial thickness with live birth: a differential impact of agonist vs antagonist ovarian stimulation protocols.Reproduction & fertility · 2026Article
- Effect of vaginal estrogen supplementation for luteal phase support in the GnRH antagonist protocol on pregnancy outcomes for IVF/ICSI cycles: a randomized controlled trial.Human reproduction open · 2026Article
- Regulated cell death in endometrial diseases: from molecular mechanisms to targeted therapies.Archives of toxicology · 2026Review
- Post-marketing safety profile of ganirelix in women: a 20-year pharmacovigilance analysis of global adverse drug event databases (2004-2024).BMC pharmacology & toxicology · 2025Article
- The effectiveness of an oral gonadotropin-releasing hormone antagonist relugolix for retained products of conception (RPOC) formed after abortion at less than 22 weeks of gestation: a retrospective study.Frontiers in medicine · 2025Article
- Reproductive outcomes of dual trigger therapy with GnRH agonist and hCG versus hCG trigger in women with diminished ovarian reserve: a retrospective study.Reproductive biology and endocrinology : RB&E · 2024Article
- Reproductive outcomes in fresh transfer cycles and antagonists with premature luteinizing and/or progesterone surge: a single center retrospective cohort study.Frontiers in endocrinology · 2024Article
- New insights for gynecological cancer therapies: from molecular mechanisms and clinical evidence to future directions.Cancer metastasis reviews · 2023Review
- Effect of Flexible Half-Dose Gonadotropin-Releasing Hormone Antagonist Protocol on in vitro Fertilization Outcome in Predicted Normal Responder: A Study Protocol for a Multicentered, Randomized, Non-Inferiority, Parallel Controlled Trial.Drug design, development and therapy · 2023Article
- Stem cell factor's role in enhancing the quality of fertilized and cloned porcine embryos for improved embryonic stem cell derivation.Frontiers in veterinary science · 2023Article
- Impact of growth hormone on IVF/ICSI outcomes and endometrial receptivity of patients undergoing GnRH antagonist protocol with fresh embryo transfer: a pilot study.Frontiers in endocrinology · 2023Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSeveral surveys have reported that patients treated with gonadotropin-releasing hormone antagonist (GnRH-ant) protocol showed a significantly lower rate of implantation and clinical pregnancy compared to GnRH agonist (GnRH-a) protocol during in vitro fertilization-fresh embryo transfer. Subsequent studies imputed this poor outcome to the negative effects of GnRH-ant on endometrial receptive. However, the mechanisms were not fully understood.
methodsThe clinical data of 2815 patients undergoing fresh embryo transfer in our center were analyzed. Human endometrial stromal cells (ESCs) from healthy women undergoing elective pregnancy termination of a normal pregnancy at 8-10 weeks gestation were treated with GnRH-analogs or imatinib (c-kit receptor inhibitor). CCK8 and Flow cytometry were used to investigated the growth ability of ESCs. Immunofluorescence staining and western blot was used to detected the target proteins.
resultsThe clinical data showed that the endometrial thickness on HCG Day were significantly lower in GnRH-ant group. Although no difference of embryo quality in these two groups, GnRH-ant group showed remarkably decreased rate of HCG positive, embryo implantation and pregnancy. Moreover, GnRH-ant significantly reduced the proliferation and induced the apoptosis of ESCs. Furthermore, the expression and activation of c-kit receptor, which played pivotal roles during embryo implantation, were observably decreased by GnRH-ant. Inhibiting the activation of c-kit by imatinib remarkably suppressed the proliferation and promoted the apoptosis of ESCs. Additionally, the phosphorylation of AKT and expression of Cyclin D1, which were closely related with cellular growth, were distinctly lessened after treating with imatinib.
conclusionsIn summary, our study showed that GnRH-ant weakened the activization of c-kit receptor by decreasing its expression, causing the impaired growth ability of ESCs. Our findings provided a new insight into the effects of GnRH-ant on endometrium.
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