Reproduction Abstracts

Introduction: The endometrium is one of the few adult tissues that heals repeatedly without scarring. On a monthly basis the endometrium undergoes cyclical episodes of proliferation, degeneration, tissue repair and remodelling in response to the ‘injury’ inflicted on it during menstruation. In women, endometrial shedding (menses) is the culmination of a cascade of inflammatory signals between uterine stromal cells and immune cells both of which have key roles in endo...

Background: The human endometrium is a dynamic, multi-cellular sex steroid-dependent tissue subject to cyclical episodes of breakdown (menses), repair and regeneration. The mechanisms responsible for initiation of menses are well characterised; the molecular and cellular changes responsible for rapid repair are poorly understood. Re-epithelialisation of the tissue is thought to involve contributions from both the stromal and epithelial compartments. A role for androgens in end...

Introduction: Hypothalamo–pituitary–testicular feedback is intact in the ovine fetus. Exogenous testosterone suppresses fetal LH and testicular steroidogenesis to maintain normal circulating testosterone concentrations. INSL3 is a non-steroidal hormone secreted by the fetal testis whose roles include facilitating testicular descent. We hypothesised that the homeostatic response to increased androgens would have a detrimental effect on fetal INSL3 expression....

Introduction: Following labour, the uterus rapidly returns to its pre-pregnancy state. Exact mechanisms underlying labour and postpartum involution are not fully understood but inflammation is understood to play a key role. It has been hypothesised that rather than initiating or propagating labour, inflammation may prime the uterus for extensive postpartum tissue repair and remodelling, in a manner akin to repair in exercising skeletal muscle. This study aims...

Introduction: Overexposure to androgens during fetal life creates offspring with a polycystic ovary syndrome (PCOS)-like phenotype. Whether this phenotype is attributable to androgens during fetal life, or estrogens via maternal/placental metabolism, remains uncertain. The potential for in utero steroidal disruption of adrenal development and function is also unclear. We have examined the adrenal during development and adulthood in response to in utero androg...