Background: We studied the cellular constituents and the expression of vascular endothelial growth factor (VEGF) and transforming growth factor-beta (TGF-beta2) in idiopathic epiretinal membranes (ERMs), attempting to correlate the presence of these growth factors with fluorescein leakage during angiography and with the amount of macular scar tissue.
Methods: Idiopathic ERMs were excised at vitrectomy in 41 consecutive cases and stained for glial fibrillary acidic protein (GFAP), vimentin, cytokeratin, desmin and actin. A subset of 13 cases for which fluorescein angiograms and colour retinal photographs were available was further studied for the presence of VEGF and TGF-beta2 in the ERMs, fluorescein leakage and amount of macular scar tissue.
Results: Of the 41 ERMs, 31 (76%) were found to be fibroglial by light microscopy; 40 (98%) stained for GFAP, 39 (95%) for vimentin, 10 (24%) for cytokeratin, 3 (7%) for desmin and 11 (27%) for actin. Of the 13 ERMs in the subset, staining was positive for VEGF in 11 (85%) and for TGF-beta2 in 11 (85%). There was no statistically significant relationship between the presence of VEGF and leakage (p = 0.68) or between the presence of TGF-beta2 and scar size (p = 0.90). When both VEGF and TGF-beta2 were present, there was likely to be leakage or a large scar, or both, which suggested that an interaction exists between the two growth factors (p = 0.057). When leakage occurred, large scars were 2.5 times less likely to be present; when no leakage occurred, large scars were 2.5 times more likely to be present (odds ratio 0.4; Yules association coefficient -0.43).
Interpretation: The cells constituting idiopathic ERMs were primarily fibroglial with minimal staining evidence for the presence of contractile proteins in their cytoplasm. VEGF and TGF-beta2 were present in 85% of specimens. Although there was no direct correlation between the presence of these growth factors and either fluorescein leakage or the abundance of scar tissue respectively, there was some evidence for the interaction of these growth factors in producing either leakage or abundance of scar tissue.