Transcriptome analysis of endometrial tissues following GnRH agonist treatment in a mouse adenomyosis model

Song Guo, Xiaowei Lu, Ruihuan Gu, Di Zhang, Yijuan Sun, Yun Feng
Drug design, development and therapy · 2017 · vol. Volume11 , pp. 695–704 · doi:10.2147/dddt.s127889 · PMID:28331289 · PMC5352156 · W2593868725
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study analyzed endometrial gene expression in a mouse adenomyosis model treated with a GnRH agonist, revealing differential regulation of genes involved in estrogen metabolism and cell cycle that may impact pregnancy outcomes.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study examined whether GnRH agonist treatment improves pregnancy outcomes and alters endometrial gene expression in a mouse model of adenomyosis. Neonatal female mice were used to induce adenomyosis, then treated with a GnRH agonist or left untreated, after which pregnancy outcomes were compared and endometrial transcriptomes were analyzed at day 4 of pregnancy using RNA sequencing (with qRT-PCR validation for three samples per group). GnRH agonist treatment reduced the deficit in fertility, increasing average live litter size relative to untreated adenomyosis, and identified 359 differentially expressed genes enriched for processes including estrogen metabolism, cell cycle regulation, and metabolite biosynthesis, with an explicit limitation of small sample size for the RNA-seq comparisons. The paper is centrally about endometriosis/adenomyosis — it specifically uses and interrogates an adenomyosis mouse model to characterize how GnRH agonists change endometrial transcriptomes and pregnancy outcomes.

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Abstract

PURPOSE: Adenomyosis is a common, benign gynecological condition of the female reproductive tract characterized by heavy menstrual bleeding and dysmenorrhea. Gonadotropin-releasing hormone (GnRH) agonists are one of the medications used in adenomyosis treatment; however, their underlying mechanisms are poorly understood. Moreover, it is difficult to obtain endometrial samples from women undergoing such treatment. To overcome this, we generated an adenomyosis mouse model, which we treated with an GnRH agonist to determine its effect on pregnancy outcomes. We also analyzed endometrial gene expression following GnRH agonist treatment to determine the mechanisms that may affect pregnancy outcome in individuals with adenomyosis. METHODS: Neonatal female mice were divided into a control group, an untreated adenomyosis group, and an adenomyosis group treated with a GnRH agonist (n=6 each). The pregnancy outcome was observed and compared among the groups. Then, three randomly chosen transcriptomes from endometrial tissues from day 4 of pregnancy were analyzed between the adenomyosis group and the GnRH agonist treatment group by RNA sequencing and quantitative reverse transcription polymerase chain reaction (PCR). RESULTS: <0.05) after GnRH agonist treatment. Three hundred and fifty-nine genes were differentially expressed in the GnRH agonist-treated group compared with the untreated group (218 were downregulated and 141 were upregulated). Differentially expressed genes were related to diverse biological processes, including estrogen metabolism, cell cycle, and metabolite biosynthesis. CONCLUSION: GnRH agonist treatment appears to improve the pregnancy outcome of adenomyosis in a mouse model. Besides pituitary down-regulation, other possible mechanisms such as the regulation of cell proliferation may play a role in this. These new insights into GnRH agonist mechanisms will be useful for future adenomyosis treatment.

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Condition tags

adenomyosisdysmenorrhea

MeSH descriptors

Adenomyosis Adenomyosis Endometrium Endometrium Gene Expression Profiling Gonadotropin-Releasing Hormone Adenomyosis Animals Animals, Newborn Disease Models, Animal Endometrium Female Gonadotropin-Releasing Hormone High-Throughput Nucleotide Sequencing Mice Pregnancy

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SciLite annotations

organisms 47
transgenic mice transgenic mice transgenic mice mus sp. transgenic mice mus sp. transgenic mice multicellular animals transgenic mice mus sp. rodents mus sp. mus sp. peanut mus sp. mus sp. mus sp. mus sp. mus sp. mus sp. mus sp. transgenic mice multicellular animals multicellular animals naine d'afrique de l'ouest transgenic mice mus sp. transgenic mice mus sp. mus sp. mus sp. humans humans transgenic mice mus sp. humans mus sp. mus sp. transgenic mice mus sp. mus sp. human mus sp. rodents human humans transgenic mice
chemicals 24
estrogen levonorgestrel palmitoyl amino acid water tamoxifen lecithin tamoxifen tamoxifen ethanol haematoxylin nitrogen nucleotide tamoxifen urea pentaglutamyl folate oxygen estrogen estradiol estradiol estrogen androgen estrone estrogen estrogen

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