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

K J A F van Kaam, J P Schouten, Annemiek Nap, A W Nap, G A J Dunselman, Patrick G. Groothuis, P G Groothuis
Human Reproduction · 2008 · vol. 23(12) , pp. 2692–2700 · doi:10.1093/humrep/den153 · PMID:18716038 · W2158463125
article OA: bronze CC0 ⤵ 60 in-corpus citations
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Deeply infiltrating endometriosis lesions contain myofibroblast-like cells, and this fibromuscular differentiation is a local environmental reaction to ectopic endometrium, distinct from TGF-beta signaling.

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Abstract

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-beta (TGF-beta) signaling is involved in this process. METHODS: FM differentiation and TGF-beta 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-beta 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-beta 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-beta signaling alone.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Animals Cell Differentiation Choristoma Choristoma Endometriosis Female Fibroblasts Fibroblasts Fibroblasts Humans Mice Mice, Nude Muscle, Smooth Muscle, Smooth Receptors, Transforming Growth Factor beta Receptors, Transforming Growth Factor beta Signal Transduction Smad2 Protein Smad2 Protein

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Cited by (50)

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