Hum. Reprod. Advance Access published online on October 5, 2007
Human Reproduction, doi:10.1093/humrep/dem262
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Endometrial cells from women with endometriosis have increased adhesion and proliferative capacity in response to extracellular matrix components: towards a mechanistic model for endometriosis progression
1 Nuffield Department of Obstetrics and Gynaecology, Level 3, The Womens Centre, John Radcliffe Hospital, Oxford OX3 9DU, UK 2 Department of Obstetrics and Gynaecology, University Hospital Gasthuisberg, Herestraat 41, 3000 Leuven, Belgium
3 Correspondence address. Tel: +44-1865-221003; Fax: +44-1865-221001; E-mail: helen.mardon{at}obs-gyn.ox.ac.uk
BACKGROUND: Endometriosis, classified as the presence of endometrial cells in ectopic sites, is a debilitating disease causing pain and infertility in
10% of women of reproductive age. It is associated with the aberrant expression of extracellular matrix (ECM) components and their receptors, integrins.
METHODS: We analysed the expression of integrins in stromal cells derived from peritoneal, ovarian and deeply infiltrating endometriotic lesions and from endometrium from women with and without endometriosis in vitro, using quantitative immunocytochemistry. The adhesive and proliferative capacity of each of the cell types in response to ECM components was assessed by in vitro assays of cell attachment and DNA synthesis.
RESULTS: We demonstrate that eutopic and ectopic endometrial stromal cells from women with endometriosis exhibit an aberrant integrin profile in vitro compared with stromal cells derived from healthy controls. In addition, the former display increased adhesion and proliferative capacity in response to specific ECM components.
CONCLUSIONS: We propose that the increased adhesive and proliferative potential of cells from endometriotic lesions may be a key feature in the pathogenesis of endometriosis. Furthermore, the elevated responsiveness of eutopic cells from women with endometriosis may contribute to the predisposition of some women to the disease.
Key words: extracellular matrix/proliferation/endometrium/endometriosis
Submitted on November 3, 2006; resubmitted on May 1, 2007; accepted on July 11, 2007.
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