Meryem İlkay KARAGÜL, Zehra Demiray ASOĞLU, Ayşe YILDIRIM
Düzce Tıp Fakültesi Dergisi - 2026;28(2):142-149
Aim: Polycystic ovary syndrome (PCOS) is associated with impaired fertility due to both ovarian dysfunction and alterations in uterine physiology. The aim of this study was to demonstrate the effect of PCOS on myometrium morphology and alpha-actin expression, which plays a role in the contraction mechanism, as well as on the ultrastructural morphology of myometrial smooth muscle cells (MSMCs). Material and Methods: Twenty-one female Sprague-Dawley rats (21 days old) were divided into control, vehicle and PCOS groups (n = 7 per group). PCOS was induced in the PCOS group by subcutaneous injections of 6 mg/100 g/day of dehydroepiandrosterone (DHEA) dissolved in 0.2 ml of sesame oil for 20 days. Light microscopic analyses of uterine tissue were performed. An ultrastructural examination of MSMCs was performed using transmission electron microscopy. Results: The PCOS group exhibited elevated epithelium thickness and stromal eosinophil infiltration. Masson trichrome staining revealed significant collagen deposition between the smooth muscle bundles in the myometrium, indicating fibrotic remodelling. Immunohistochemical analysis revealed decreased alpha-actin expression in the PCOS group. Ultrastructurally, MSMCs in the PCOS group demonstrated enlarged perinuclear spaces, while the morphology of dense bodies remained normal. Conclusion: PCOS induces significant remodelling of the myometrium, including increased collagen deposition, vascular dilation and early ultrastructural stress changes. These findings suggest that uterine dysfunction in PCOS may be caused by subtle yet functionally significant alterations to myometrial architecture. Further research incorporating functional contractility assays and contraction-related molecular pathways is required to clarify the mechanisms linking myometrial remodelling to impaired reproductive outcomes in PCOS.
