Endometriosis is a common benign estrogen dependent chronic gynecological disorder associated with pelvic pain and infertility. It is characterized by the presence of uterine endometrial tissue outside of normal environment. The prevalence of pelvic endometriosis approaches 6-10% of general female population in the reproductive age. How uterine endometrial tissue following retrograde menstruation is able to migrate towards and to invade extrauterine sites is presently unclear. However, signalling pathways involved in regulation of proliferation and migration can be differentially regulated in ectopic lesions and eutiopic endometrium from patients with endometriosis, compared to the control healthy population. As a model system we use primary cultures of stromal-epithelial cells obtained from tissue samples isolated from healthy women and patients with endometriosis from eutopic sites (uterus) and ectopic lesions (ovary).
The project aims to investigate the molecular mechanisms involved in the establishment of endometriosis and in particular:
- Regulation of cell migration and the role of Raf-1/ROCKII signalling pathway
- To analyze the role of MAPK pathway, as regulator of cell proliferation in endometriosis
- To investigate the role of Raf-1/ROCKII signalling pathway in regulation of cell proliferation in our in vitro cell system