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    Arrangement of myofibroblastic and smooth muscle-like cells in superficial peritoneal endometriosis and a possible role of transforming growth factor beta 1 (TGFβ1) in myofibroblastic metaplasia (2019)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Ibrahim, Mohamed Gamal
    Sillem, Martin
    Plendl, Johanna (WE 1)
    Taube, Eliane T.
    Schüring, Andreas
    Götte, Martin
    Chiantera, Vito
    Sehouli, Jalid
    Mechsner, Sylvia
    Quelle
    Archives of gynecology and obstetrics
    Bandzählung: 299
    Heftzählung: 2
    Seiten: 489 – 499
    ISSN: 0932-0067
    Sprache
    Englisch
    Verweise
    URL (Volltext): https://link.springer.com/article/10.1007/s00404-018-4995-y
    DOI: 10.1007/s00404-018-4995-y
    Pubmed: 30523440
    Kontakt
    Institut für Veterinär-Anatomie

    Koserstr. 20
    14195 Berlin
    +49 30 838 75784
    anatomie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    Purpose:
    Superficial peritoneal endometriotic (pEM) lesions are composed of endometrial glands and stroma, in addition to a third component-myofibroblasts and smooth muscles (SM)-like cells. The latter develops secondary to a metaplasia. In this study, we characterised the third component cells in pEM according to differentiation markers in different micro-compartments. Furthermore, a possible effect of TGFβ1 on myofibroblastic metaplasia in endometriotic epithelial cells was studied.

    Methods:
    Seventy-six premenopausal patients were included. Peritoneal biopsies were excised from EM patients (n = 23), unaffected peritoneum (peritoneum from EM patients but without EM components, n = 5/23) and non-EM patients (n = 10). All peritoneal biopsies were immunolabeled for ASMA, calponin, collagen I, desmin, TGFß receptor 1 (R1), R2 and R3 in addition to ultrastructure examination by transmission electron microscopy (TEM) (n = 1). TGFß1 level was measured in peritoneal fluid (PF) (EM, n = 19 and non-EM, n = 13) collected during laparoscopy. Furthermore, TGFß1 effect on myofibroblastic metaplasia was studied in vitro.

    Results:
    At the centre of pEM lesions, calponin immunolabeling outweighs the collagen I while in the periphery the reverse occurs. SM-like cells expressing desmin predominate at the periphery, while ASMA immunolabeling was detectable in all micro-compartments. Both indicate an abundance of myofibroblasts at the centre of pEM lesions and SM-like cells in the periphery. Although activated TGFß1 in PF did not differ between EM and non-EM, it inhibited the cell proliferation of the endometriotic epithelial cells and induced an upregulation in ASMA and collagen IA2 expression as well.

    Conclusion:
    The abundance of the myofibroblasts and SM-like cells points to a myofibroblastic metaplasia in pEM. Both cells are differentially arranged in the different micro-compartments of pEM lesions, with increasing cell maturity towards the periphery of the lesion. Furthermore, TGFß1 may play a role in the myofibroblastic metaplasia of the endometriotic epithelial cells. These findings provide a better insight in the micro-milieu in EM lesions, where most of the disease dynamics occur.