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

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. Overall design: Four fertile and four subfertile Pgrcre/+Rosa26mTmG/+ mice with endometriosis, and four sham mice for each group of endometriosis mice as control. These mice underwent either surgery to induce endometriosis or sham surgery. Fertile sham and mice with endometriosis were used one month after surgery, while subfertile ones were used three months after surgery. RNA-Seq analysis and identification of differential expressed genes and pathways in the ectopic lesions and eutopic uteri from mice with endometriosis and sham mice at day of pregnancy 3.5.