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Transcriptomic changes in eutopic endometrium and ectopic lesions in mouse model during progression of endometriosis-related infertility

ABSTRACT: In this study, we performed transcriptomic analysis in ectopic lesions and eutopic endometrial tissues from both fertile and subfertile mice with endometriosis. We identified the positive correlation of the gene signatures between the mouse and human in ectopic lesions. Conserved gene networks were activated in all the ectopic lesions including estradiol, immune, fibrosis, and angiogenesis pathways. The interactions mediated through hormone, cytokine, and growth factor as well as their corresponding receptors were predicted between the ectopic and eutopic endometrium. EGF and WNT signaling were more suppressed in the eutopic endometrium from subfertile mice. Our results revealed that our mouse endometriosis model recapitulates the important transcriptomic changes of endometriosis progression in human ectopic lesions including the essential regulator network and intensive inter-communications between ectopic and eutopic endometrium. Our preclinical animal model for endometriosis will be invaluable to understand etiology and pathophysiology on endometriosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE240392 | GEO | 2024/05/29

REPOSITORIES: GEO

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Project description:Endometriosis is associated with aberrant gene expression in the eutopic endometrium of women with disease. To determine if the development of endometriotic lesions directly impacts eutopic endometrial gene expression, we sequentially analyzed the eutopic endometrium across the time course of disease progression in a baboon model of induced disease. Endometriosis was induced in baboons by intraperitoneal inoculation of autologous menstrual endometrium. Eutopic endometria were collected at 9-11 days postovulation) in five time points: 1, 3, 6-7, 10-12, and 15-16 months after disease induction and compared with tissue from disease-free baboons. We used microarrays to identify differentially expressed genes between time points. Sequential analysis of the same animals during disease progression demonstrated an early disease insult and a transitory dominance of an estrogenic phenotype. However, as the disease progressed, a progesterone-resistant phenotype became evident. Endometriosis was experimentally induced in Papio anubis female baboons (n = 4) by intraperitoneal inoculation with menstrual endometrium on two consecutive menstrual cycles. Baboons with spontaneous endometriosis (n = 2) were also included in this study with an unknown duration of disease. Control endometrium was similarly harvested from animals (n = 4) with no previous surgeries and with no visible disease. The progression of disease was monitored in each animal by consecutive laparoscopies and video recording at 1 (n = 2), 3 (n = 4), 6-7 (n = 4), 10-12, (n = 4), and 15-16 (n = 3) months after inoculation during a window of 9-11 days postovulation. Eutopic endometrial tissues were harvested and were snap frozen in liquid nitrogen for RNA extraction. Additionally, menstrual endometrium was harvested on Days 1-2 of menses using a Unimar Pipelle (Cooper Surgical Inc., Shelton, CT) immediately prior to laparoscopy. Blood samples were collected daily from days 7 through 16 postmenstruation of menstrual cycles.

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Transcriptomic changes in eutopic endometrium and ectopic lesions in mouse model during progression of endometriosis-related infertility

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