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Marie-Luce Bochaton-Piallat, Anastasios D. Kapetanios, Guy Donati, Mireille Redard, Giulio Gabbiani, Constantin J. Pournaras; TGF-β1, TGF-β Receptor II and ED-A Fibronectin Expression in Myofibroblast of Vitreoretinopathy. Invest. Ophthalmol. Vis. Sci. 2000;41(8):2336-2342.
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purpose. Formation of scarlike epiretinal membranes (ERMs) constitutes
potentially the end stage of evolution of proliferative
vitreoretinopathy (PVR) and proliferative diabetic retinopathy (PDR).
Among various cellular populations, ERMs contain cells with contractile
features typical of myofibroblasts. The current study was conducted to
investigate the presence of transforming growth factor (TGF)-β1,
TGF-β receptor II (RII) and ED-A fibronectin (FN), the main inducers
of myofibroblastic differentiation in ERMs in PDR and PVR.
methods. Samples of ERM were obtained from 23 patients during microsurgery for
PVR or PDR. Electron microscopy, immunohistochemistry, and confocal
microscopy with antibodies recognizing α-smooth muscle (SM) actin,
desmin, TGF-β1, TGF-β receptors I and II, and ED-A FN were
results. α-SM actin was detected in all ERMs, whereas desmin was present in
50% of the cases. ED-A FN was expressed in all ERMs in close relation
with α-SM actin–positive myofibroblasts. In addition, TGF-β1 and
TGF-β R II were always present, TGF-β RII being expressed in bothα
-SM actin–positive and negative fibroblastic cells.
conclusions. Myofibroblast accumulation is a key event in ERM-associated traction
retinal detachment occurring during PVR and PDR. The current results
suggest that the presence of α-SM actin–positive myofibroblasts is
probably dependent on the concomitant neoexpression of TGF-β1,
TGF-β RII, and ED-A FN. The results furnish new data on the mechanism
of α-SM actin stimulation in fibroblasts in a human pathologic
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