Abstract
Endometriosis is an inflammatory gynecological disorder among reproductive-aged women caused by the engraftment and proliferation of endometrial cells outside the uterus, most commonly in the pelvis. It is thought that the disease arises primarily from retrograde menstruation where cells from the endometrium travel through the fallopian tubes to the peritoneal cavity. However, migration of endometriosis-derived cells to distant organs outside of the peritoneal cavity have not been explored. In the present study, we developed and validated a mouse model of disseminated endometriosis using syngeneic DsRed endometrial tissue introduced into the peritoneum of immunocompetent mice. Flow cytometry and immunofluorescence analysis, demonstrated the presence of endometriosis-derived cells in multiple organs (including lung, spleen, liver and brain) in the murine endometriosis model. Immunostaining revealed the presence of DsRed+/CD45− cells in brain, liver and lung. Engraftment occurred in all experimental animals examined. Cells from endometriotic lesions are capable of migration to and engraftment of multiple organs outside of the peritoneal cavity. Micrometastasis of endometriosis is a novel and frequent phenomenon. These data suggest that widespread dissemination of endometriosis may be common, clinically unrecognized and contribute to the diffuse clinical manifestations of this disease.
Highlights
Endometriosis is a common gynecological disorder among reproductive aged women (6–10%) [1] due to the deposition and growth of endometrial cells outside the uterus [2, 3]
To determine whether endometriosis lesions have cells with the ability to migrate from experimental endometriosis to the lung, we performed Fluorescence Activated Cell Sorting (FACS)
We demonstrate here that endometriosis-derived cells are capable of migration to extrapelvic organs including the lung, spleen, liver and brain
Summary
Endometriosis is a common gynecological disorder among reproductive aged women (6–10%) [1] due to the deposition and growth of endometrial cells outside the uterus [2, 3]. The most widely accepted theory of its etiology is ectopic implantation, or Sampson’s theory, which proposes that endometrial cells are shed out of the uterus through retrograde menstruation, thereby gaining access to and implanting on pelvic structures [9]. Implants of endometriosis outside of the peritoneal cavity, in women affected by Mayer-Rokitansky-Kuster-Hauser’s syndrome (absent uterus) or reports of endometriosis in men cannot be explained by these theories [10, 11]. The theory of vascular dissemination suggests that endometrial cells may enter the uterine vasculature or lymphatic system at menstruation and are transported to other sites [12]. Our group has described a stem cell origin of endometriosis; endometriosis arises from ectopic differentiation of circulating mesenchymal stem cells [7, 13,14,15,16]
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