Endometriose - eine Stammzellerkrankung?

Subscribe to RSS DOI: 10.1055/s-2003-42276 © Georg Thieme Verlag Stuttgart · New York Endometriose - eine Stammzellerkrankung? Endometriosis - A Stem Cell Disease?Publication History Publication Date: 23 September 2003 (online) Zusammenfassung Es ist allgemein akzeptiert, dass die Endometriose eine Östrogen-abhängige und chronisch-rezidivierende Erkrankung ist. Ihre Ätiologie und Pathogenese sind letztendlich unbekannt. Es ist jedoch wahrscheinlich, dass in vielen Fällen retrograd menstruierte Endometriumszellen der Urprung der Endometrioseerkrankung sind. In dieser Arbeit diskutieren wir ein Modell, nach dem die retrograd menstruierten Zellen ein Gemisch verschiedener Entwicklungsstadien von Endometriumszellen darstellen, die zum Teil anhand von Markerproteinen wie z. B. den Cadherinen (Zelladhäsionsproteine) oder Cytokeratin (Intermediärfilamentproteinen) charakterisiert werden können. In Analogie zu bisherigen Erkenntnissen aus anderen Zellsystemen postulieren wir, dass in diesem Zellgemisch auch Zellen mit Stammzellcharakter bzw. Plastizität (d. h. Zellen, die noch Differenzierungspotenzial besitzen) vorhanden sind. Auf der einen Seite können sich diese Zellen als Zellpopulation selbst erhalten, auf der anderen Seite müssten diese Zellen mit Stammzellcharakter/Plastizität sich in differenzierte Tochterzellen entwickeln und so neue Endometrioseherde bilden können. Zellen unterschiedlicher Entwicklungsstadien befinden sich sowohl in tief infiltrierenden Endometrioseherden (z. B. Darm) aber auch in Peritonealbiopsien. Demnach könnten die Zellen mit dem postulierten Stammzellcharakter bzw. der Plastizität die rezidivierende Ausgangszellpopulation der Endometriose sein. Abstract Endometriosis is an estrogen-dependent and chronic disease with an unknown etiology and pathogenesis. It is however likely and well accepted that retrograd menstruation of endometrial cells into the pelvic cavity is the origin of this disease in many cases. Here we discuss a model in which retrogradly menstruated endometrial cells have different inherent developmental properties because they represent in fact a mixture of different developmental cell stages. These stages can be distinguished in part by the expression of marker proteins such as cytokeratin (intermediate filament protein of epithial cells) or E-cadherin (intercellular adhesion protein of epithelial cells and metastasis suppressor molecule). Cytokeratin-positive E-cadherin negative cells, for example, would be less differentiated epithelial cells than cytokeratin-positive E-cadherin positive cells. In analogy to findings in other cell systems we assume that the cells which are undifferentiated or not fully differentiated still have the potential to give rise to differentiated daughter cells and, on the other hand, could be maintained as a pool of rather undifferentiated cells and capable of self renewal. This feature would be similar to stem cells (SC) and cells with plasticity. Interestingly we find epithelial cells of different developmental stages in deep infiltrating (e. g. of colon) or peritoneal endometriotic lesions. Therefore we conclude that less differentiated cells in retrogradly menstruated endometrial cell populations possibly representing SC features or plasticity might be the cellular source of primary endometriotic lesions and those present in lesions may contribute to the persistence of the disease by detaching and forming secondary lesions. 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