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1 From the Department of Pathology, University of Geneva; and the 2 Department of Ophthalmology and Clinical Neurosciences, University Hospitals, Geneva Medical School, Switzerland.
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)-ß1, TGF-ß 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 
-smooth muscle (SM) actin,
desmin, TGF-ß1, TGF-ß receptors I and II, and ED-A FN were
performed.
RESULTS. -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 -SM actin–positive myofibroblasts. In addition, TGF-ß1 and
TGF-ß R II were always present, TGF-ß RII being expressed in both
-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 -SM actin–positive myofibroblasts is
probably dependent on the concomitant neoexpression of TGF-ß1,
TGF-ß RII, and ED-A FN. The results furnish new data on the mechanism
of -SM actin stimulation in fibroblasts in a human pathologic
setting.
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