Searchable abstracts of presentations at key conferences on reproductive biology and medicine

ra0001p006 | Uterus | WCRB2014

Estrogen-dependent modulation of neuroinflammation in endometriosis

Greaves Erin , Horne Andrew W , Saunders Philippa T K

Introduction: Endometriosis is an estrogen-dependent inflammatory disorder, associated with debilitating pelvic pain. We believe the pain is due to neuroinflammation: growth of sensory neurons and their subsequent hypersensitisation by macrophage-derived cytokines within the lesion. We explored the regulation of neuroinflammation by estrogen receptor (ER) modulators.Materials and methods: Peritoneum and lesions were collected from women with and without ...

ra0003p027 | (1) | SRF2016

Targeting lactate metabolism can be a novel therapeutic for the treatment of endometriosis

Ahmad Syed Furquan , Greaves Erin , Saunders Philippa , Horne Andrew

Introduction: Endometriosis is a chronic, hormone-dependent disorder characterized by the establishment and growth of endometrial tissue in extra-uterine sites, typically within the peritoneal cavity and causes debilitating pain. We have shown that peritoneal mesothelial cells recovered from the women with endometriosis have an altered energy metabolism with increased biosynthesis of lactate as a result of increased aerobic glycolysis. We hypothesize that ectopic endometrial t...

ra0001p295 | (1) | WCRB2014

Investigating the role of androgens in endometriosis

Simitsidellis Ioannis , Greaves Erin , Collins Frances , Horne Andrew W , Saunders Philippa T K

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 e...