Stefania Mosele1, Christina Anna Stratopoulou1, Alessandra Camboni2, Jacques Donnez3, Marie-Madeleine Dolmans4. 1. Pôle de Recherche en Gynécologie, Institut de Recherche Expérimentale et Clinique, Université Catholique de Louvain, Brussels, Belgium. 2. Pôle de Recherche en Gynécologie, Institut de Recherche Expérimentale et Clinique, Université Catholique de Louvain, Brussels, Belgium; Anatomopathology Department, Cliniques Universitaires Saint-Luc, Brussels, Belgium. 3. Professor EM, Université Catholique de Louvain, Brussels, Belgium, Société de Recherche pour l'Infertilité, Brussels, Belgium. 4. Pôle de Recherche en Gynécologie, Institut de Recherche Expérimentale et Clinique, Université Catholique de Louvain, Brussels, Belgium; Gynecology Department, Cliniques Universitaires Saint-Luc, Brussels, Belgium. Electronic address: marie-madeleine.dolmans@uclouvain.be.
Abstract
RESEARCH QUESTION: Do platelets aggregate in adenomyotic lesions and participate in adenomyosis pathogenesis and related fibrosis? DESIGN: Eutopic and ectopic endometrium from 17 patients with adenomyosis and endometrium from 23 healthy controls were collected. Immunohistochemical analyses of platelet marker CD41, transforming growth factor beta 1 (TGF-β1) and vascular endothelial growth factor (VEGF) were performed to investigate aggregation and activation of platelets in the stroma. Picrosirius staining was carried out to evaluate the extent of fibrotic tissue. RESULTS: Stroma in the control group showed higher CD41 staining levels than ectopic stroma from patients with adenomyosis (P < 0.001). In patients with adenomyosis, eutopic stroma expressed more extensive CD41 staining than ectopic stroma (P < 0.0001). Stroma in the control group exhibited higher TGF-β1 expression than eutopic and ectopic stroma from adenomyosis patients (P = 0.009 and P < 0.0001). Stroma in the control group also expressed higher VEGF levels than ectopic stroma from patients with adenomyosis (P < 0.001). In patients with adenomyosis, eutopic stroma showed higher VEGF expression than ectopic stroma (P = 0.021). Stroma in ectopic endometrium from adenomyosis patients displayed greater Picrosirius staining compared with both eutopic stroma from adenomyosis patients and stroma in the control group (P < 0.0001). CONCLUSION: The results of this study did not detect a primary role for platelet activation or aggregation in the pathophysiological process of adenomyosis. Higher rates of collagen fibres were found in adenomyotic lesions, likely to be related to a TGF-β1-independent pathway. Collagen fibre deposition was more extensive in adenomyotic lesions, consistent with fibrosis.
RESEARCH QUESTION: Do platelets aggregate in adenomyotic lesions and participate in adenomyosis pathogenesis and related fibrosis? DESIGN: Eutopic and ectopic endometrium from 17 patients with adenomyosis and endometrium from 23 healthy controls were collected. Immunohistochemical analyses of platelet marker CD41, transforming growth factor beta 1 (TGF-β1) and vascular endothelial growth factor (VEGF) were performed to investigate aggregation and activation of platelets in the stroma. Picrosirius staining was carried out to evaluate the extent of fibrotic tissue. RESULTS: Stroma in the control group showed higher CD41 staining levels than ectopic stroma from patients with adenomyosis (P < 0.001). In patients with adenomyosis, eutopic stroma expressed more extensive CD41 staining than ectopic stroma (P < 0.0001). Stroma in the control group exhibited higher TGF-β1 expression than eutopic and ectopic stroma from adenomyosispatients (P = 0.009 and P < 0.0001). Stroma in the control group also expressed higher VEGF levels than ectopic stroma from patients with adenomyosis (P < 0.001). In patients with adenomyosis, eutopic stroma showed higher VEGF expression than ectopic stroma (P = 0.021). Stroma in ectopic endometrium from adenomyosispatients displayed greater Picrosirius staining compared with both eutopic stroma from adenomyosispatients and stroma in the control group (P < 0.0001). CONCLUSION: The results of this study did not detect a primary role for platelet activation or aggregation in the pathophysiological process of adenomyosis. Higher rates of collagen fibres were found in adenomyotic lesions, likely to be related to a TGF-β1-independent pathway. Collagen fibre deposition was more extensive in adenomyotic lesions, consistent with fibrosis.