Abstract
Endometriosis is characterized by the presence of endometrial tissue outside the uterus. While endometriotic tissue is commonly localized in the pelvic cavity, it can also be found in distant sites, including the brain. The origin and pathophysiology of tissue migration is poorly understood; retrograde menstruation is thought to be the cause, although the presence of endometrium at distant sites is not explained by this hypothesis. To determine whether dissemination occurs via the bloodstream in women with endometriosis, we analyzed circulating blood for the presence of endometrial cells. Circulating endometrial stromal cells were identified only in women with endometriosis but not in controls, while endometrial epithelial cells were not identified in the circulation of either group. Our results support the hypothesis that endometrial stromal cells may migrate through circulation and promote the pathophysiology of endometriosis. The detection of these cells in circulation creates avenues for the development of less invasive diagnostic tools for the disease, and opens possibilities for further study of the origin of endometriosis.
Highlights
Endometriosis is a benign disease characterized by the growth of endometrial tissue outside of the uterine cavity which affects approximately 15% of pre-menopausal women [1,2]
Rodent models of endometriosis demonstrated that endometriotic cells migrated from lesions to eutopic endometrium [12], suggesting that they migrated through extravasation
We found a mean of 14.75 circulating endometrial cells (CECs; range 0–57) in the group with endometriosis (n = 8) and no CECs in the four healthy donors
Summary
Endometriosis is a benign disease characterized by the growth of endometrial tissue outside of the uterine cavity which affects approximately 15% of pre-menopausal women [1,2]. Rodent models of endometriosis demonstrated that endometriotic cells migrated from lesions to eutopic endometrium [12], suggesting that they migrated through extravasation This process seems to be regulated by an epithelial-mesenchymal transition (EMT), since the migrating cells express aberrant epithelial markers in the stroma [12]. EMT could play a role in the migration of endometrial LGR5+CK+ cells, since they overexpressed MMP12, a matrix metalloproteinase involved in the degradation of the extracellular matrix and involved in the EMT process [16] Taken together, these findings suggest that endometrial cells might be able to migrate from eutopic endometrium to ectopic sites through circulation thanks to an EMT process
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