Reproduction Abstracts

Introduction: Androgen receptors (AR) have been detected in the human endometrium throughout the menstrual cycle and are reported to regulate expression of genes associated with cellular proliferation and cell-cycle regulation. Endometriosis is defined by establishment and growth of endometrial tissue in ectopic locations (typically on the peritoneal wall); patients often experience pain and infertility. In the current study we have used human tissue and a new mouse model of endometriosis to investigate the expression of AR and the potential impact of androgens on cellular proliferation and gene expression.

Materials and methods: Tissue samples (eutopic endometrium, peritoneum and endometriotic lesions) were obtained from women attending a pelvic pain clinic who gave informed consent. Equivalent tissue samples were collected from a recently established mouse model of endometriosis. Some mice were injected with dihydrotestosterone (DHT). Messenger RNA concentrations and proteins were investigated by RT-PCR and immunofluorescence.

Results and discussion: Immunoexpression of AR in normal mouse uterus was localised to stromal fibroblasts consistent with that reported for human endometrium. In contrast to normal uterus, in endometriotic lesions recovered from both women and mice AR was localised to stromal and epithelial compartments. There was minimal co-expression of AR and proliferation markers in endometriotic cells. DHT treatment altered the expression of putative AR-regulated genes in the mouse uterus. These results demonstrate that AR expression in a mouse model of endometriosis parallels human disease and provides a platform for investigating the impact of androgens/selective AR ligands on endometriosis.