Research

Ubiquitin is associated with the survival of ectopic stromal cells in endometriosis

Romina S Ilad¹ , Steven D Fleming¹ , Catherine R Bebington² and Christopher R Murphy³

¹  Department of Obstetrics and Gynaecology, University of Sydney, New South Wales, Australia

²  Department of Reproductive Medicine, Westmead Hospital, New South Wales, Australia

³  Department of Anatomy and Histology, University of Sydney, New South Wales, Australia

author email corresponding author email

Reproductive Biology and Endocrinology 2004, 2:69doi:10.1186/1477-7827-2-69

Published:	25 September 2004

Abstract

Background

Endometriosis is a condition that affects women of reproductive age, where the glandular and/or stromal tissues from the eutopic endometrium implant in ectopic locations. It is well established that the survival of ectopic implants is due to lower levels of apoptosis, but no consensus exists as to which pathway/s this is mediated by. The ubiquitin protein shares a similar sequence homology to an anti-apoptotic protein called BAG-1 and is expressed in the normal endometrium. Currently, no studies have been conducted to determine ubiquitin expression and its possible anti-apoptotic effects in endometriosis.

Methods

Archived endometrial tissues from endometriosis patients and women undergoing laparoscopic diagnosis (controls) from January 2000 to July 2003 at Westmead Hospital were examined, where 14 cases of endometriosis and 55 controls were included in the study.

Results

Both the ubiquitin protein and apoptosis were expressed in both glandular and stromal cells throughout the menstrual cycle of the eutopic endometrium, in which ubiquitin exhibited a cyclic expression, reaching a peak in late proliferative phase. In contrast, ubiquitin was predominantly expressed in cells of stromal origin in endometriosis, was no longer regulated by a cyclic pattern and was associated with an aberrant level of cell survival.

Conclusions

For the first time, this study shows that ubiquitin is expressed in endometriotic cells and may contribute to a reduced sensitivity of ectopic endometrial tissue to apoptosis. These findings also suggest that stromal cells contribute differentially to the development of ectopic endometrial tissue.