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Purpose: Fibrous epiretinal membranes (ERMs) result from inappropriate proliferation, migration and differentiation of several cell types including myofibroblasts. They occur at the endstage of proliferative and idiopathic vitreoretinopathy, and proliferative diabetic retinopathy. Myofibroblasts exhibit contractile features that are typical of granulation tissue during wound healing and fibrocontractive diseases and are responsible for granulation tissue remodeling and retraction. The marker of myofibroblasts is the expression of alpha-smooth muscle actin (alpha-SMA). Transforming growth factor-beta1 (TGF-beta1) and ED-A fibronectin are key players of the complex process of myofibroblast differentiation. Methods: Samples of ERM were studied by electron microscopy, immunohistochemistry, and confocal microscopy with antibodies specific for alpha-SMA, vimentin, TGF-beta1, TGF-beta receptor II and EDA- fibronectin. Results: The presence of alpha-SM actin-positive myofibroblasts was associated with the expression of vimentin, TGF-beta1, TGF-beta receptor II, and ED-A fibronectin in all types of ERMs. Conclusions: The results furnish new data on the mechanism of alpha-SM actin stimulation in fibroblasts in a human pathologic setting. |
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