Study of the mechanisms coupling tissue breakdown and regeneration during menstruation in a murine model of human endometrial xenografts

Menstruation is a remarkable physiological process that couples tissue degradation and regeneration. Although globally regulated by cyclic fluctuations of ovarian steroids concentration, endometrial remodeling is tightly controlled in space and time by molecular mechanisms that are only partially understood. Inappropriate control of uterine homeostasis and/or menstruation is associated with pathologies such as infertility, endometriosis and dysfunctional uterine bleeding. The aim of this work was to better understand these regulatory mechanisms by using a murine model of human endometrium xenograft mimicking menstruation. In a first study, we found that hypoxia is not required for the induction of menstrual breakdown and early tissue repair. In a second study, we measured changes in xenograft volume and showed that hormone withdrawal alone triggered epithelial cell proliferation and tissue repair but without increased volume of the graft.