Autor: |
Richards EG; Cardiovascular and Metabolic Sciences, Lerner Research Institute; Women's Health Institute, Cleveland Clinic; richare@ccf.org., Rehmer JM; Women's Health Institute, Cleveland Clinic., Mathes MA; Department of Obstetrics and Gynecology, 983255 Nebraska Medical Center, University of Nebraska Medical Center., Esakov EL; Cardiovascular and Metabolic Sciences, Lerner Research Institute; Women's Health Institute, Cleveland Clinic., Braley C; Cardiovascular and Metabolic Sciences, Lerner Research Institute; Women's Health Institute, Cleveland Clinic., Joehlin-Price A; Anatomic Pathology, Cleveland Clinic., Chiesa-Vottero A; Anatomic Pathology, Cleveland Clinic., Reizes O; Cardiovascular and Metabolic Sciences, Lerner Research Institute; Women's Health Institute, Cleveland Clinic; Gynecologic Oncology, Women's Health Institute and Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Cleveland Clinic; reizeso@ccf.org. |
Abstrakt: |
Endometriosis is a leading cause of pelvic pain and infertility. It is defined by the presence of endometrial tissue in extrauterine locations. The development of novel therapies and diagnostic tools for endometriosis has been limited due in part to challenges in studying the disease. Outside of primates, few mammals menstruate, and none develop spontaneous endometriosis. Rodent models are popular but require artificial induction of endometriosis, with many utilizing either immunocompromised mice or surgically induced disease. Recently, more attention has been given to models involving intraperitoneal injection. We present a murine model of endometriosis that integrates several features of existing endometriosis models into a novel, simplified system that relies on microscopic quantification in lieu of subjective grading. In this model, we perform hormonal stimulation of donor mice, intraperitoneal injection, systematic abdominal survey and tissue harvest, and histologic quantification that can be performed and verified at any time after necropsy. This model requires minimal resources and training; does not require expertise by lab technicians in murine survival surgery or in the identification of gross endometriotic lesions; can be used in immunocompromised, immunocompetent, and/or mutant mice; and reliably creates endometriotic lesions that are histologically consistent with human endometriotic disease. |