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Hum. Reprod. Advance Access originally published online on August 20, 2008
Human Reproduction 2008 23(12):2692-2700; doi:10.1093/humrep/den153
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© The Author 2008. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Fibromuscular differentiation in deeply infiltrating endometriosis is a reaction of resident fibroblasts to the presence of ectopic endometrium

K.J.A.F. van Kaam1,2,4, J.P. Schouten1,2, A.W. Nap1,2, G.A.J. Dunselman1,2 and P.G. Groothuis3

1 Research Institute GROW, University of Maastricht/University Hospital Maastricht, Maastricht, The Netherlands 2 Department of Obstetrics and Gynaecology, University of Maastricht/University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, The Netherlands 3 Department of Pharmacology, Organon Biosciences, PO Box 20, 5340 BH Oss, The Netherlands

4Correspondence address. E-mail: kimvankaam{at}yahoo.com

BACKGROUND: In this study, we characterized the fibromuscular (FM) tissue, typical of deeply infiltrating endometriosis, investigated which cells are responsible for the FM reaction and evaluated whether transforming growth factor-β (TGF-β) signaling is involved in this process.

METHODS: FM differentiation and TGF-β signaling were assessed in deeply infiltrating endometriosis lesions (n = 20) and a nude mouse model of endometriosis 1, 2, 3 and 4 weeks post-transplantation. The FM reaction was evaluated by immunohistochemistry using different markers of FM and smooth muscle cell differentiation (vimentin, desmin, alpha-smooth muscle actin, smooth muscle myosin heavy chain). TGF-β signaling was assessed by immunostaining for its receptors and phosphorylated Smad.

RESULTS: Deeply infiltrating endometriosis lesions contain myofibroblast-like cells that express multiple markers of FM differentiation. Expression of TGF-β receptors and phospho-Smad was more pronounced in the endometrial component of the lesions than in the FM component. In the nude mouse model, alpha-smooth muscle actin expression was observed in murine fibroblasts surrounding the lesion, but not in human endometrial stroma.

CONCLUSIONS: FM differentiation in deeply infiltrating endometriosis is the result of a reaction of the local environment to the presence of ectopic endometrium. It shares characteristics with pathological wound healing, but cannot be explained by TGF-β signaling alone.

Key words: transforming growth factor-β/endometriosis/ectopic endometrium/smooth muscle metaplasia/fibromuscular differentiation

Submitted on August 15, 2008; resubmitted on January 22, 2008; accepted on February 22, 2008.


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